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1.
Li X Li J Cheng K Lin Q Wang D Zhang H An H Gao M Chen A 《Cell biochemistry and biophysics》2011,61(2):427-434
We evaluated the effect of low-intensity pulsed ultrasound (LIPUS) on MMP-13 and MAPKs expression in rabbit knee osteoarthritis
(OA). For this purpose, 18 New Zealand white rabbits were randomly and equally divided into O + L, O – L, and SO groups. In
O + L group, animals underwent right back leg ACLT operation and LIPUS radiation. In O − L group, animals underwent ACLT but
no LIPUS treatment. In SO (control) group, animals underwent sham operation without LIPUS. After 6 weeks, we assessed the
pathologic changes in the articular surface of femoral condyle and compared using Mankin scores. Also, expression of type-II
collagen, MMP-13, ERK1/2, p38, and JNK was measured by Western blot. Compared with controls, Mankin scores were higher in
O + L (P < 0.05)/O − L (P < 0.01) groups. Compared with O + L group, score was higher in O − L group (P < 0.05). Compared with controls, type-II collagen expression was less in O + L/O − L groups, with more significant decrease
in O − L group (P < 0.05). Contrarily, expression of MMP-13, p-ERK1/2, and p-p38 was enhanced in O + L/O − L groups as compared with controls,
with more significant increase in O − L group (P < 0.01). Compared with O + L group, expression was higher in O − L group (P < 0.05). We, therefore, concluded that LIPUS application promoted cartilage repair in OA through the downregulation of MMP-13,
ERK1/2, and p38. 相似文献
2.
《Saudi Journal of Biological Sciences》2020,27(11):3046-3059
This study aimed to investigate the long-term scar hypertrophy in the rabbit transplanted oral mucosa and scrotal skin with changed matrix environment, as well as the scar location expression, quantitative analysis of matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) and biomechanical changes in the transplanted tissues. The split-thickness skin grafts were collected from the oral mucosas and scrotal skins of 30 male rabbits, and prepared into reelpipes for autologous transplantation into the rabbit back muscular tissues. Samples were collected to carry out elastic tensile mechanical detection and histological observation. The maximum longitudinal tensile displacement of scrotal skin before 8 weeks of transplantation was greater than that after 8 weeks of transplantation (P < 0.05). The expression intensities of MMP-2 and TIMP-2 in the oral mucosa and in scrotal skin at 2 W time point were higher than those at To time point (P < 0.05). The expression quantities of TIMP-2 in oral mucosa and scrotal skin during 8–24 W were higher than those of MMP-2 (P < 0.05). At 8 W time point, the TIMP-2/MMP-2 ratio in scrotal skin was higher than that in oral mucosa (P < 0.05). MMP-2 and TIMP-2 expression in normal oral mucosa and scrotal skin is weak, but their expression is remarkably up-regulated after 2 weeks of transplantation, revealing that scar formation was related to the high expression of MMP-2 and TIMP-2. At the 8th–24th weeks, the AOD values of TIMP-2 in oral mucosa and scrotal skin are apparently higher than those of MMP-2; moreover, the TIMP-2/MMP-2 ratio in scrotal skin at the 8th week was higher than that in oral mucosa, which can well explain the earlier scar formation in scrotal skin than in oral mucosa, and it also suggests that the different expression levels between TIMP-2 and MMP-2 may account for the important cause of scar formation. 相似文献
3.
Ventricular assist devices may function as a bridge to recovery or heart transplantation, however, little is known about its
mechanisms. This study examined the role of matrix metalloproteinases (MMP)-tissue inhibitors of metalloproteinases (TIMP)
axis in the process of recovery after unloading in a rat ischemic-induce heart failure (HF) model. Myocardial infarction model
was created with the coronary artery ligation. The infarcted rats hearts were unloaded by heterotopic cardiac transplantation
(n = 14). 2 weeks later, the function of normal and infarcted hearts with or without loading was evaluated by Langendorff perfusion
model. The hearts were then harvested and prepared for the study of expression of MMPs and TIMPs. Developed pressure in the
unloading group was higher than the loading group (P = 0.0074). Unloading increased the ratio of TIMP-1–MMP-1(1.38 ± 0.11 vs. 0.76 ± 0.09, P < 0.05), TIMP-2–MMP-2 (1.06 ± 0.10 vs. 0.33 ± 0.07, P < 0.01), TIMP-3–MMP-9(1.07 ± 0.08 vs. 0.59 ± 0.06, P < 0.05). Although MMP-1, 2, 9 were downregulated (P < 0.01, 0.01, 0.05, respectively), TIMP-2 and TIMP-3 upregulated (P < 0.01, 0.05, respectively), MMP-7 and TIMP-1 was not affected significantly. The infarcted cardiac function could be improved
by unloading. It was attributed to downregulation of MMP-1, 2 and 9, and upregulation of TIMP-2 and -3, and furthermore, the
ratio of TIMPs to MMPs was increased, which might be more sensitive than sole MMPs or TIMPs for the judgment of myocardial
matrix homeostasis. 相似文献
4.
Binata Joddar Rebecca J. G. Shaffer Rashmeet K. Reen Keith J. Gooch 《Biomechanics and modeling in mechanobiology》2011,10(2):161-175
Ex vivo culture of arteries and veins is an established tool for investigating mechanically induced remodeling. Porcine saphenous
veins (PSV) cultured ex vivo with a venous mechanical environment, serum-supplemented cell-culture medium and standard cell-culture
conditions (5% CO2 and 95% balance air ~140 mmHg pO2) develop intimal hyperplasia (IH), increased cellular proliferation, decreased compliance and exhibit inward eutrophic remodeling
thereby suggesting that nonmechanical factors stimulate some changes observed ex vivo. Herein we explore the contribution
of exposure to greater than venous pO2 and serum to these changes in cultured veins. Removing serum from culture medium did not inhibit development of IH, but did
reduce cellular proliferation and inward eutrophic remodeling. In contrast, veins perfused using reduced pO2 (75 mmHg) showed reduced IH. Among the statically cultured vessels, veins cultured at arterial pO2 (95 mmHg) and above showed IH as well as increase in proliferation and vessel weight compared to fresh veins; veins cultured
at venous pO2 did not. Taken together, these data suggest that exposure of SV to arterial pO2 stimulates IH and cellular proliferation independent of changes in the mechanical environment, which might provide insight
into the etiology of IH in SV used as arterial grafts. 相似文献
5.
Yongjie Xu Wenmin Yu Yuanzhu Xiong Hongtao Xie Zhuqing Ren Dequan Xu Minggang Lei Bo Zuo Xiaoting Feng 《Molecular biology reports》2011,38(5):2903-2909
SRPK3 is a protein kinase belonging to serine/arginine protein kinases (SRPK) family, which phosphorylates serine/arginine
repeat-containing proteins, and is controlled by a muscle-specific enhancer directly regulated by MEF2. In this study, a full-length
cDNA of the porcine SRPK3 gene encoding a 566 amino acid protein was isolated. It contains 14 exons over approximately 4.3 kb. The deduced amino acid
sequence of porcine SRPK3 contains a bipartite kinase domain, and shows high similarities to their corresponding human and
cattle homologues. Tissue distribution analysis indicated that porcine SRPK3 mRNAs are highly expressed in heart and skeletal muscle especially in uterus and parorchis, but at low level in brain, stomach,
small intestine, and ovary. Expression pattern of SRPK3 was similar in Large White and Chinese Meishan breeds. Both the two breeds had the highest expression levels at fetal 65 days
(P < 0.01), and decreased while the age increased until 60 days old, then increased at 120 days (P < 0.01) and decreased at 180 days (P < 0.05). However, at fetal 65 days, the mRNA abundance of SRPK3 in Large White was 12.5-fold higher than in Meishan pigs (P < 0.01), whereas at 180 days, the abundance in Meishan was 3.4-fold higher than in Large White pigs (P < 0.01). These results suggest that the SRPK3 gene might be an important gene of skeletal muscle development and also provides basic molecular information useful for further
studies on its roles in porcine skeletal muscle. 相似文献
6.
We determined the effect of atorvastatin on myocardial apoptosis and caspase-8 activation following coronary microembolization
(CME) in a rat model. For this, 50 rats were randomly and equally divided into CME; sham-operated (control); atorvastatin
lavage; gastric lavage control; and caspase-8 inhibitor (CHO) groups. In CME animals, a microembolization ball was injected
through the left ventricle. Sham animals were injected with normal saline (NS). Atorvastatin group received atorvastatin gastric
lavage once-a-day, 1 week before surgery. Gastric lavage controls had similar lavage with NS. CHO group was i.p-injected (CHO:
10 mg/kg) 30 min before surgery. Cardiac indices in each group were determined by echocardiography 6-h postoperatively. TUNEL
assay and western blot were used for myocardial apoptosis and expression of caspases-3/-8, respectively. Echocardiography
data show that left ventricular ejection fraction (LVEF) in CME group was significantly decreased (P < 0.05) compared with sham controls. Besides, left ventricular fractional shortening (FS) and cardiac output (CO) were also
decreased with an increase in left ventricular end-diastolic dimension (LVEDd). Atorvastatin and CHO animals had significantly
improved (P < 0.05) cardiac function compared with CME group. Myocardial apoptosis and activation levels of caspases-3/-8 were significantly
increased (P < 0.05) compared with sham; myocardial apoptosis and activation levels of caspases-3/-8 were significantly decreased (P < 0.05) in atorvastatin and CHO groups compared with CME group. In conclusion, atorvastatin pretreatment suppressed post-CME
myocardial apoptosis and improved cardiac function through the blockade of a myocardial death receptor-mediated apoptotic
pathway. 相似文献
7.
Elmas E Hölzer L Lang S Popp T Kälsch T Wolpert C Brueckmann M Borggrefe M 《Cytokine》2008,43(2):138-142
Aims. Ventricular fibrillation (VF) in the setting of acute myocardial infarction (AMI) is the leading cause of sudden cardiac death. A potential role of intrinsic, subclinical inflammatory states in patients suffering from ischemia-related VF has not been investigated yet. The aim of the present study was (i) to examine serum levels of proinflammatory markers in VF survivors and (ii) to evaluate basal and lipopolysaccharide (LPS)-stimulated interleukin-8-mRNA (IL-8-mRNA) levels in patients with and without VF complicating AMI. Methods. Twenty-five patients with a history of VF during AMI and a control group of 25 AMI patients without VF were included. Blood samples were taken remote from AMI with a mean of 590 days. Circulating serum levels of IL-8, IL-6, soluble E-selectin (sE-selectin), tissue factor activity (TFA), tissue inhibitor of matrix-metalloproteinase-1 (TIMP-1) and matrix-metalloproteinase-9 (MMP-9) were measured. Mononuclear cells were isolated by density gradient centrifugation. The cells were stimulated with lipopolysaccharide (LPS) from Escherichia coli (700 ng/mL). IL-8-mRNA levels in mononuclear cells were determined by a colorimetric mRNA quantification assay. Results. Serum levels (median; range) of IL-8 (VF: 2.24 pg/mL; <0.10–19.3 pg/mL versus controls: 0.10 pg/mL; <0.10–7.7 pg/mL; p = 0.014), IL-6 (VF: 0.68 pg/mL; <0.05–2.9 pg/mL versus controls: 0.23 pg/mL; <0.05–1.8 pg/mL; p = 0.042) and TIMP-1 (VF: 229 ng/mL; 144–348 ng/mL versus controls: 186 ng/mL; 126–263 ng/mL; p = 0.014) were significantly higher among patients with VF as compared to controls. Baseline IL-8-mRNA concentrations of blood mononuclear cells were significantly higher among patients with VF (257 amol/mL; 52–2672 amol/mL) as compared to patients without VF (37 amol/mL, 3.2–770 amol/mL; p < 0.01). IL-8-mRNA levels after LPS-challenge were significantly higher among patients with VF (3503 amol/mL; 215–13,573 amol/mL) than in patients without VF (1003 amol/mL; 208–3386 amol/mL; p < 0.01). Conclusions. Circulating IL-8, IL-6, and TIMP-1 concentrations as well as IL-8-mRNA expression in mononuclear cells at baseline and after LPS-challenge are increased among patients with a history of VF in the setting of AMI as compared to patients without VF. These findings indicate an enhanced inflammatory response to a proinflammatory stimulus in VF survivors. The magnitude of this increased acute phase reactants may indicate a novel pathway of arrhythmogenesis in patients with AMI. 相似文献
8.
Hideyuki Maeda Hisashi Nagai Genzou Takemura Kaori Shintani-Ishida Masaaki Komatsu Sayoko Ogura Toshihiko Aki Mikiayasu Shirai Ichiro Kuwahira Ken-ichi Yoshida 《生物化学与生物物理学报:疾病的分子基础》2013,1832(8):1159-1166
Sleep apnea syndrome (SAS) is considered to be associated with heart failure (HF). It is known that autophagy is induced in various heart diseases thereby promotes survival, but its excess may be maladaptive. Intermittent hypoxia (IH) plays pivotal role in the pathogenesis of SAS. We aimed to clarify the relationships among IH, autophagy, and HF. Rats underwent IH at a rate of 20 cycles/h (nadir of 4% O2 to peak of 21% O2 with 0% CO2) or normal air breathing (control) for 8 h/d for 3 weeks. IH increased the cardiac LC3II/LC3I ratio. The IH induced upregulation of LC3II was attenuated by the administration of an inhibitor of autophagosome formation 3-methyladenine (3-MA), but enhanced by an inhibitor of autophagosome–lysosome fusion chloroquine (CQ), showing enhanced autophagic flux in IH hearts. Electron microscopy confirmed an increase in autophagosomes and lysosomes in IH. With 3-MA or CQ, IH induced progressive deterioration of fractional shortening (FS) on echocardiography over 3 weeks, although IH, 3-MA, or CQ alone had no effects. With CQ, IH for 4 weeks increased serum troponin T levels, reflecting necrosis. Western blotting analyses showed dephosphorylation of Akt and mammalian target of rapamycin (mTOR) at Akt (Ser2448, 2481) sites, suggesting the activation of autophagy via Akt inactivation. Conclusions. IH-mediated autophagy maintains contractile function, whereas when autophagy is inhibited, IH induces systolic dysfunction due to myocyte necrosis. General significance. This study highlighted the potential implications of autophagy in cardio-protection in early SAS patients without comorbidity, reproduced in normal rats by 3 ~ 4 weeks of IH. 相似文献
9.
10.
Chae CH Jung SL An SH Jung CK Nam SN Kim HT 《Journal of physiology and biochemistry》2011,67(2):235-241
We investigated the effects of treadmill exercise performed regularly for 6 weeks on the levels of nerve growth factor (NGF),
tyrosine kinase A and p75 receptors, phosphatidylinositol 3-kinase (PI3-K), mitogen-activated protein kinase/extracellular
signal-regulated kinase (Erk) 1,2, cyclic AMP response element-binding protein (CREB), and caspase-3 in the soleus of rats
with streptozotocin (STZ)-induced diabetes. Thirty-two male Sprague–Dawley rats were divided into the following four groups:
(1) normal control group (NCG; n = 8), (2) normal exercise group (NEG; n = 8), (3) diabetes control group (DCG; n = 8), and (4) diabetes exercise group (DEG; n = 8). Diabetes was induced by intraperitoneal injection of STZ (55 mg/kg dissolved in 0.05 M citrate buffer, pH 4.5). Rats
were subjected to treadmill exercise 5 days a week for 6 weeks. The protein level of NGF significantly increased in the NEG
and DEG (p < 0.001), whereas the levels of tyrosine kinase A and p75 receptors significantly increased in the NEG (p < 0.001). The levels of t-PI3-K, p-PI3-K, and p-CREB, and the p-CREB/t-CREB ratio significantly increased in the NEG (p < 0.001, respectively). The p-PI3-K/t-PI3-K ratio significantly increased in the DEG (p < 0.001). The p-Erk1/t-Erk1 ratio significantly increased in the NEG (p < 0.001), whereas the p-Erk2/t-Erk2 ratio significantly decreased in the DCG and DEG (p < 0.001). The caspase-3 level significantly increased in the DCG compared with that in the DEG (p < 0.001). These results suggest that treadmill exercise increases NGF levels and accelerates p-PI3-K activation in order
to suppress apoptotic cell death in the soleus muscle of diabetic rats. 相似文献
11.
The purpose of this study was to assess the value of cytokeratin 19 (CK19) and matrix metalloproteinase 2 (MMP-2) in predicting
lymph node metastasis (LNM) and survival after curative resection in hepatocellular carcinoma (HCC) patients. Expression of
CK19 and MMP-2 in tumor tissue was assessed through immunohistochemical staining of tissue microarrays (TMAs), which were
constructed using samples from HCC patients with (n = 123) and without (n = 145) LNM. Positive CK19 expression was correlated with LNM (P < 0.001), satellite lesions (P = 0.016), and lymph node location (P = 0.039). High MMP-2 expression correlated with LNM (P < 0.001), UICC T stage (P = 0.023), and Edmondson grade (P = 0.022). Moreover, CK19 expression correlated with MMP-2 expression (P = 0.033). CK19 and MMP-2 expression were predictive of HCC LNM (AUC: 0.640; 95% CI: 0.572–0.707; P < 0.001 and AUC: 0.611; 95% CI: 0.544–0.679; P = 0.002, respectively). CK19 and MMP-2 expression were independent prognostic factors for disease-free survival (P = 0.031 and P = 0.012, respectively) and overall survival (P = 0.013 and P = 0.018, respectively) in HCC patients with LNM. CK19 expression (P < 0.001), MMP-2 expression (P = 0.006), and UICC T stage (P < 0.001) were independent risk factors for developing LNM in HCC. These findings show that CK19 and MMP-2 expression may
be beneficial in predicting HCC LNM and survival. 相似文献
12.
Alipour M Gholami MR Jafari Anarkooli I Sohrabi D Tajki J Pourheidar M 《Cellular and molecular neurobiology》2011,31(5):765-773
The present work was designed to investigate the potential protective effects of post-ischemic treatment with aminoguanidine
(AG) on sciatic nerve ischemia/reperfusion (I/R) injury in rat. Seventy-two rats were divided into 12 groups (n = 6). We used ischemia model in these groups by occluding the right common iliac and femoral arteries for 3 h with a silk
suture 6-0 using slipknot technique. Treatment groups (2, 4, 6, 8, 10, and 12) received 150 mg/kg AG intraperitoneally 24 h
after induction of ischemia. After certain time intervals of reperfusion (2, 4, 7, 14, and 28 days), the function of the hind
limb was assessed using behavioral scores based on gait, racing reflex, toe spread, pinch sensitivity, paw position, and grasp.
After euthanasia, sciatic nerves were removed at the end of reperfusion times and sections were cut at 5 μm, then were stained
for light microscopy studies and graded for ischemic fiber degeneration (IFD), edema, and apoptosis. Maximal behavioral deficit
occurred at 7 days of reperfusion. The comparison of behavioral score pertaining to the control and AG groups revealed significant
differences and showed also a better time course in recovery (P < 0.05). Other than 3 and 4 groups, the amount of edema in AG treatment groups showed significant differences compared with
control groups (P < 0.05). IFD was also significantly decreased in the AG treatment groups than controls. Most importantly, I/R-induced apoptosis
were improved significantly on the 4th, 7th, and 14th days of reperfusion in AG-treated groups compared to controls. In conclusion, our findings suggest that post-ischemic
administration of AG exhibits protective effect against sciatic nerve I/R injury. 相似文献
13.
Roya Kolahdouz-Mohammadi Farzad Shidfar Sepideh Khodaverdi Tahereh Arablou Sahel Heidari Nesa Rashidi Ali-Akbar Delbandi 《Journal of cellular and molecular medicine》2021,25(2):1116-1127
Endometriosis is an inflammatory disease affecting reproductive-aged women. Immunologic disturbance, as well as inflammation, have crucial roles in the pathogenesis of endometriosis. In this study, we evaluated the effects of resveratrol treatment on expression of monocyte chemotactic protein-1 (MCP-1), interleukin-6 (IL-6), IL-8, and regulated upon activation, normal T cell expressed and secreted (RANTES) in endometrial stromal cells from patients with endometriosis compared with non-endometriotic controls. Thirteen eutopic (EuESCs) and nine ectopic (EESCs) endometrial stromal cells from endometriotic patients as well as eleven endometrial stromal cells from non-endometriotic controls (CESCs) were treated with resveratrol (100 μmol/L) or ethanol, and gene and/or protein expression of MCP-1, IL-6, IL-8 and RANTES was examined at 6, 24 and 48 hours following treatment in the cells from all origins. Resveratrol treatment significantly reduced gene and protein expression of MCP-1, IL-6, and IL-8 in EuESCs and EESCs compared with CESCs (P < .05-.001, P < .05-.001 and P < .05-<.01, respectively), and this reduction was more noticeable in EESCs than EuESCs (P < .05-<.001). Besides, resveratrol treatment significantly reduced RANTES protein expression in EESCs in all time intervals (P < .05). Resveratrol treatment significantly reduced the expression of MCP-1, IL-6, IL-8 and RANTES in EESCs. 相似文献
14.
Mel S. Lee Hon-Kan Yip Chih-Chao Yang John Y. Chiang Tien-Hung Huang Yi-Chen Li Kuan-Hung Chen Pei-Hsun Sung 《Journal of cellular and molecular medicine》2021,25(16):7675-7689
This study tested the hypothesis that therapy with double overexpression of miR-19a-3p and miR-20a-5p (miRDOE) to human inducible pluripotent stem cell–derived mesenchymal stem cells (iPS-MSCs) was superior to iPS-MSCs alone for preserving renal function in rat with pre-existing chronic kidney disease (CKD), followed by ischaemia-reperfusion (IR) injury. In vitro study demonstrated that the protein expressions of oxidative stress (NOX-1/NOX-2/NOX4/oxidized protein/p22phox), inflammatory downstream signalling (TLR2&4/MyD88/TRAF6/IKK-ß/p-NFκB/IL-1ß/IL-6/MMP-9) and cell apoptosis/death signalling (cleaved caspase-3/mitochondrial Bax/p-ERKs/p-JNK/p-p38) at time-points of 24-hour/48-hour cell cultures were significantly increased in p-Cresol-treated NRK-52E cells than in the control that was significantly reversed by miR-19a-3p-transfected iPS-MSC (all P < .001). Animals were categorized into group 1 (sham-operated control), group 2 (CKD-IR), group 3 (CKD-IR + oligo-miRDOE of iPS-MSCs/6.0 ×105/intra-renal artery transfusion/3 hours after IR procedure), group 4 (CKD-IR + iPS-MSCs) and group 5 (CKD-IR + miRDOE of iPS-MSCs/6.0 ×105/intra-renal artery transfusion/3 hour after IR procedure). By day 35, the creatinine/BUN levels were lowest in group 1, highest in group 2 and significantly lower in group 5 than in groups 3 and 4 (all P < .0001) but they showed no difference between the latter two groups. The protein expressions of oxidative stress, inflammatory downstream signalling and cell apoptosis/death signalling exhibited an identical pattern of creatinine level among the five groups (all P < .00001). Also, the microscopic findings demonstrated that the kidney injury score/fibrotic area/number of inflammatory cells (CD14+/CD68+) exhibited an identical pattern of creatine level (all P < .0001). The miRDOE of iPS-MSCs was superior to iPS-MSCs for preserving the residual kidney function and architecture in CKD-IR rat. 相似文献
15.
Toghyani M Toghyani M Shivazad M Gheisari A Bahadoran R 《Biological trace element research》2012,146(2):171-180
This study was conducted to determine the effects of dietary supplementation with Cr nicotinate and Cr chloride and their
optimum inclusion rate on performance, carcass traits, meat oxidative stability, serum metabolites, hematological parameters,
and liver chromium concentration in heat-stressed broilers. A total number of 420, 1-day-old male broiler chicks were randomly
assigned to seven treatments with four replicates of 15 chicks. The dietary treatments consisted of the basal diet supplemented
with 0 (control), 500, 1,000, and 1,500 μg/kg Cr in the form of Cr nicotinate and Cr chloride. Chicks were raised for 6 weeks
in heat stress condition (33 ± 2°C). Supplements of organic and inorganic Cr particularly at 1,500 μg/kg incorporation increased
feed consumption (P < 0.05) and body mass gain of broilers (P < 0.01). Cr supplementation increased carcass yield and decreased abdominal fat (P < 0.01). Supplementation of 1,500 μg/kg Cr nicotinate (P < 0.05) enhanced liver Cr concentration. Storage time increased lipid oxidation of meat (P < 0.01). Cr decreased lipid oxidation of breast and thigh muscles over 2 (P < 0.01) or 6 (P < 0.05) days of storage time. Birds fed 1,500 μg/kg Cr nicotinate, had lower concentration of serum glucose and triglyceride
at 21 days (P < 0.05). Hematological parameters tested at 21 and 42 days, were not influenced. The results suggested that dietary Cr supplementation
regardless of its source have a positive effect on productive, and carcass traits, also enhances oxidative stability of refrigerated
meat in broilers reared under heat stress conditions. 相似文献
16.
Testosterone and its synthetic derivatives anabolic–androgenic steroids have been shown to increase skeletal muscle work capacity
and fatigue resistance, but the molecular basis for these effects remains uncertain. Since muscle performance has been related
to redox status of exercising muscles, this investigation was aimed at testing whether a treatment with suprapharmacological
doses of the anabolic–androgenic steroid stanozolol, (2 mg/kg body weight, 5 days/week, for 8 weeks), either alone or in conjunction
with treadmill training (12 weeks), enhanced antioxidant defences in rat muscles. Stanozolol treatment did not modify thiobarbituric
acid reactive substances and glutathione content in soleus and extensor digitorum longus (EDL) homogenates. In soleus from
sedentary rats, superoxide dismutase and glutathione reductase activities were increased by 25% (P < 0.05) and by 40% (P < 0.01) after stanozolol administration, whereas catalase and glutathione peroxidase activities were not modified. This response
was similar to that induced by training alone. In EDL from sedentary rats, stanozolol increased only superoxide dismutase
activity (20%, P < 0.05). In no case, the effects of steroid administration and training were additive. HSP72 levels were up-regulated in
soleus (1.5-fold, P < 0.01) and EDL (threefold, P < 0.001) following training but remained unchanged after stanozolol treatment. Endurance capacity, assessed in a treadmill
endurance test, was similar for treated and control rats. We conclude that stanozolol treatment increases antioxidant capacity
in selected skeletal muscles from sedentary rats. However, the steroid was not effective in improving endurance capacity or
enhancing the training effects on muscle antioxidant defence systems. 相似文献
17.
Collins D Walpole C Ryan E Winter D Baird A Stewart G 《The Journal of membrane biology》2011,239(3):123-130
The process of urea nitrogen salvaging plays a vital role in the symbiotic relationship between mammals and their intestinal
bacteria. The first step in this process requires the movement of urea from the mammalian bloodstream into the gastrointestinal
tract lumen via specialized proteins known as facilitative urea transporters. In this study, we examined both transepithelial
urea fluxes and urea transporter protein abundance along the length of the rat gastrointestinal tract. Urea flux experiments
that used rat gastrointestinal tissues showed significantly higher transepithelial urea transport was present in caecum and
proximal colon (P < 0.01, n = 8, analysis of variance [ANOVA]). This large urea flux was significantly inhibited by 1,3,dimethylurea (P < 0.001, n = 8, ANOVA) and thiourea (P < 0.05, n = 6, unpaired t-test), both known blockers of facilitative urea transporters. Immunoblotting analysis failed to detect any UT-A protein within
rat gastrointestinal tissue protein samples. In contrast, a 30-kDa UT-B1 protein was strongly detected in both caecum and
proximal colon samples at significantly higher levels compared to the rest of the gastrointestinal tract (P < 0.01, n = 4, ANOVA). We therefore concluded that UT-B1 mediates the transepithelial movement of urea that occurs in specific distal
regions of the rat gastrointestinal tract. 相似文献
18.
Amine transporters are major target for development of various pharmacological agents to treat behavioral disorders. Serotonin
transporters (SERT) have been implicated in the etiology of depression and drugs acting on SERT can be effective in treating
depression. The aim of the present study was to study the in vivo effect of various antidepressants on [3H]paroxetine binding to SERT in regions of rat brain. Rats were treated with tricyclic antidepressant (TCAs) such as amitriptyline
(AMI), serotonin/norepinephrine reuptake inhibitor (SNRIs) such as clomipramine (CMI), and selective serotonin reuptake inhibitors
(SSRIs) such as fluoxetine (FLX) and citalopram (CIT) (10 mg/kg body wt.) for 30 days. Density of SERT was measured in cortex
and hippocampus using [3H]paroxetine (0.03–1.0 nM) in presence and absence of 10 μM fluoxetine as displacer. It was observed that the density of cortical
SERT was significantly decreased with CMI (68%, P < 0.0001), FLX (67%, P < 0.0001), CIT (54%, P < 0.0001), and AMI (52%, P < 0.0001) treatment, when compared to the density of 120.7 ± 4.0 fmol/mg protein in control rats, without altering the affinity
(Kd) of [3H]paroxetine to the transporters. The density of SERT in hippocampus was also significantly decreased with FLX (65%, P < 0.0001), CMI (54%, P < 0.0001), CIT (52%, P < 0.0001) and AMI (46%, P < 0.0001) treatment, when compared to the density of 74.0 ± 2.6 fmol/mg protein in control rats, without altering the affinity
of [3H]paroxetine to the transporters. Displacement study showed high affinity for CMI > CIT > FLX. The results suggest that chronic
antidepressant treatment significantly down-regulates both cortical and hippocampal SERT in rat brain and SSRIs have high
affinity for SERT than TCAs. 相似文献
19.
The calpain system, a Ca2+-activated protease family, plays an important role in postmortem tenderization of skeletal muscle due to its involvement
in the degradation of important myofibrillar and associated proteins, as well as in cytoskeletal remodeling and regulation
of muscle growth. In this study, we quantified the expression of calpastatin (CAST) in two Chinese chicken breeds (mountainous black-bone chicken breed (MB) and a commercial meat type chicken breed (S01)),
to discern the tissue and age-related specific expression pattern and its potential role on muscle tissue metabolism. Real-time
quantitative PCR (RT-qPCR) assay was developed for accurate measurement of CAST mRNA levels in various tissues from chicken with different ages (0, 2, 4, 6, 8, 10, and 12 week). CAST mRNA was detected in collected organs. The heart and leg muscle tissues had the highest expression of CAST than other tissues from the same chicken (P < 0.01). Age-related expression pattern of CAST gene was evident in breast muscle, liver, and brain tissues (P < 0.05), but not in heart and leg muscle tissues (P > 0.05). Overall, the CAST mRNA level exhibited a “rise-decline-rise-decline” developmental change in breast muscle and liver, with the highest expression
at 2 weeks and the lowest expression at 8 weeks. The S01 chicken had significantly higher expression of CAST in breast muscle and heart than the MB chicken (P < 0.05) at 10 weeks. Our results suggested the CAST expression may be related to muscle fiber development. 相似文献
20.
Michele M. Castro Elen Rizzi Cibele M. Prado Marcos A. Rossi Jose E. Tanus-Santos Raquel Fernanda Gerlach 《Matrix biology》2010,29(3):194-201
Structural vascular changes in two-kidney, one-clip (2K-1C) hypertension may result from increased matrix metalloproteinase (MMP)-2 activity. MMP-2 activation is regulated by other MMPs, including transmembrane-MMPs, and by tissue inhibitors of MMPs (TIMPs). We have investigated the localization of MMP-2, -9, -14, and TIMPs 1–4 in hypertensive aortas and measured their levels by zymography/Western blotting and immunohistochemistry. Gelatinolytic activity was assayed in tissues by in situ zymography. Sham-operated and 2K-1C hypertensive rats were treated with doxycycline (or vehicle) for 8 weeks, and the systolic blood pressure was monitored weekly. Doxycycline attenuated 2K-1C hypertension (165 ± 11.7 mmHg versus 213 ± 7.9 mm Hg in hypertensive controls, P < 0.01), and completely prevented increase in the thicknesses of the media and the intima in 2K-1C animals (P < 0.01). Increased amounts of MMP-2, -9, and -14 were found in hypertensive aortas, as well as enhanced gelatinolytic activity. A gradient in the localization of MMP-2, -9, and -14 was found, with increased amounts detected in the intima, at sites with higher gelatinolytic activity. Doxycycline attenuated hypertension induced increases in all the 3 investigated MMPs in both the media and the intima (all P < 0.05), but it did not change the amounts of TIMPs 1–4 (P > 0.05). Therefore, an imbalance between increased amounts of MMPs at the tissue level without a corresponding increase in the quantities of TIMPs, particularly in the intima and inner media layers, appears to account for the increased proteolytic activity found in 2K-1C hypertension-induced maladaptive vascular remodeling. 相似文献