Betanin alleviates oxidative stress through the Nrf2 signaling pathway in the liver of STZ-induced diabetic rats

Background

Continuing hyperglycemia causes and exacerbate oxidative stress. Betanin as the principal pigment of red beet root has antioxidant, anti-inflammatory, and anti-diabetic properties. The purpose of this study was to investigate the potency of betanin on antioxidant defense in STZ-induced diabetic rats’ livers.

Methods

STZ at a single dose of 60 mg/kg body weight was intraperitoneally injected and betanin (10, 20, and 40 mg/kg/day) was administered orally for 28 days. Malondialdehyde (MDA), total antioxidant capacity (TAC), protein carbonyl (PC) levels, and the enzyme activity of superoxide dismutase (SOD), catalases and glutathione peroxidases (GPx) were evaluated in the liver. Furthermore, gene expression of Nrf2 and mentioned antioxidant enzymes were measured by Real-time PCR.

Results

Betanin (10 and 20 mg/kg) significantly reduced PC levels and increased antioxidant enzyme activity in diabetic rats compared to the control diabetic group (P?<?0.01). In comparison to the diabetic control group, all studied genes expression in diabetic rats were increased significantly with betanin at doses of 10 and 20 mg/kg (P?<?0.02). The increase in gene expression at 20 mg/kg of betanin was significantly stronger than others (P?<?0.015) except for the catalase (P?=?0.201), that was almost the same. Moreover, treatment of diabetic rats with 20 mg/kg of betanin could significantly increase TAC levels (P?<?0.05) and decrease MDA levels (P?<?0.001) compared to diabetic control group.

Conclusions

Betanin could increase the antioxidant capacity of liver tissue associated with the Nrf2-mediated pathway in a dose-dependent manner.

     

Comparative In Vivo Evaluations of Curcumin and Its Analog Difluorinated Curcumin Against Cisplatin-Induced Nephrotoxicity

Curcumin, a polyphenol, has pharmacological effects including antioxidant, anti-inflammatory and anti-cancer features. In this study, we have performed comparative in vivo evaluations of CDF (curcumin difluorinated) and curcumin in cisplatin-induced nephrotoxicity in rats. Male Wistar rats were divided into four groups: (1) Control; (2) Cisplatin (7 mg/kg body wt, intraperitoneal as a single dose); (3) Cisplatin and CDF (50 mg/rat/day; for 12 days); (4) Cisplatin and curcumin (50 mg/rat/day), for 12 days). Cisplatin treated rats exhibited kidney injury manifested by increased serum N-urea and creatinine (P?<?0.001). Kidney from cisplatin treated rats also exhibited significant increase in malondialdehyde (MDA) and 8-isoprostane levels (P?<?0.001). Treatment with CDF and curcumin prevented the rise in serum N-urea, creatinine, MDA and 8-isoprostane as compared to experimental control group in kidney (P?<?0.05). Compared to curcumin, CDF had greater potential in suppressing cisplatin-induced pro-inflammatory factors NF-κB and COX-2 as well as downstream markers Nrf2 and HO-1 (P?<?0.05) in kidney. The analysis on anion transport markers (OAT1 and OAT3) showed a similar trend (CDF?>?curcumin). CDF could reduce the expression of multi-drug resistance markers OCT1, OCT2, MRP2 and MRP4 to a much greater extent than curcumin (P?<?0.05). We also demonstrate that CDF influenced the expression of p-mTOR, p-p70S6K1, p-4E-BP1 and p-Akt. These data suggest that CDF can potentially be used to reduce the chemotherapy induced nephrotoxicity thereby enhancing the therapeutic window of cisplatin. The results also proved that compared to curcumin, CDF has superior protective effect in nephrotoxicity.     

The Beneficial Effect of Probiotics Supplementation on Penicillin-Induced Focal Seizure in Rats

The focal epilepsy is a chronic neurological brain disorder which affects millions of people in the world. There is emerging evidence that changes in the gut microbiota may have effects on epileptic seizures. In the present study, we examined the effect of probiotics on penicillin-induced focal seizure model in rats. Male Wistar Albino rats (n: 21) were randomly divided into three groups: control (no medication), penicillin and penicillin?+?probiotic. Probiotic VSL#3 (12.86 bn living bacteria/kg/day) was given by gavage for 30 days. The seizures were induced by intracortical injection of penicillin G (500 IU) into the cortex. An ECoG recordings were made for 180 min after penicillin G application. The spike frequency and the amplitude were used to assess the severity of seizures. Tumor necrosis factor (TNF-α), nitric oxide (NO) and interleukin (IL-6) levels in the brain were studied biochemically. Our results indicated that probiotic supplementation improved focal seizures through increasing the latency (p?<?0.001) and decreasing the spike frequency (p?<?0.01) compared to the penicillin group. Penicillin-induced seizure in rats significantly enhanced TNF-α (p?<?0.01), NO (p?<?0.01) and IL-6 (p?<?0.05) compared to the control. Probiotic supplementation significantly decreased IL-6 (p?<?0.05), TNF-α (p?<?0.01) and NO (p?<?0.001) compared to the penicillin group. When the body weights were compared before and after the experiment, there was no difference between the control and penicillin groups, but it was observed that the body weight decreased after probiotic supplementation in the penicillin?+?probiotic group. Probiotic supplementation may have anti-seizure effect by reducing proinflammatory cytokine and NO levels in epileptic rat brain.

     

Protective Role of Cactus Cladodes Extract on Sodium Dichromate-Induced Testicular Injury and Oxidative Stress in Rats

Cactus (Opuntia ficus-indica) is a xerophyte plant that belongs to the Cactaceae family. The present study was designed to investigate the possible protective effects of cactus cladodes extract (CCE) on sodium dichromate-induced testis damage in adult male Wistar rats. For this purpose, CCE at a dose of 100 mg/kg was orally administrated, followed by 10 mg/kg sodium dichromate (intraperitoneal injection). After 40 days of treatment, the rats were sacrificed, and the testes were excised for histological, lipid peroxidation (LPO), and antioxidant enzyme analyses. Sodium dichromate treatment significantly (P?<?0.01) decreased the body, testis, and accessory sex organ weights, sperm count and motility, and serum testosterone level. In addition, histological analysis revealed pronounced morphological alterations with tubular necrosis and reduction in the number of gametes in the lumen of the seminiferous tubules of sodium dichromate-intoxicated rats. Furthermore, exposure to sodium dichromate significantly (P?<?0.01) increased LPO level and decreased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in testis. Interestingly, pretreatment with CCE significantly (P?<?0.01) restored the serum testosterone level, sperm count, and motility to the levels of the control group. Moreover, CCE administration was capable of reducing the elevated level of LPO and significantly (P?<?0.01) increased SOD, CAT, and GPx activities in testis. Cactus cladodes supplementation minimized oxidative damage and reversed the impairment of spermatogenesis and testosterone production induced by sodium dichromate in the rat testis.     

Effect of 3:7 ratio of Astragalus total saponins and Curcumin on the diabetic nephropathy rats model

Objective

Study the effect of the 3:7 ratio of Astragalus total saponins and Curcumin on the model of diabetic nephropathy rats, and explore its mechanisms.

Selenomethionine administration decreases the oxidative stress induced by post mortem ischemia in the heart,liver and kidneys of rats

Selenium is an essential element in human and animal metabolism integrated into the catalytic site of glutathione peroxidase (GPX1), an antioxidant enzyme that protects cells from damage caused by reactive oxygen species (ROS). Oxidative stress refers the imbalance between ROS and antioxidant defense systems. It generates alterations of DNA, proteins and lipid peroxidation. The imbalance occurs particularly during ischemia and lack of postmortem perfusion. This mechanism is of relevance in transplant organs, affecting their survival. The aim of this research is to evaluate the effect of seleno-methionine (SeMet) as a protective agent against postmortem ischemia injury in transplant organs. Wistar rats were orally administered with SeMet. After sacrifice, liver, heart and kidney samples were collected at different postmortem intervals (PMIs). SeMet administration produced a significant increase of Se concentration in the liver (65%, p?<?0.001), heart (40%, p?<?0.01) and kidneys (45%, p?<?0.05). Levels of the oxidative stress marker malondialdehyde (MDA) decreased significantly compared to control in the heart (0.21?±?0.04 vs. 0.12?±?0.02 mmol g^?1) and kidneys (0.41?±?0.02 vs. 0.24?±?0.03 mmol g^?1) in a PMI of 1–12 h (p?<?0.01). After SeMet administration for 21 days, a significant increase in GPX1 activity was observed in the liver (80%, p?<?0.001), kidneys (74%, p?<?0.01) and heart (35%, p?<?0.05). SeMet administration to rats significantly decreased the oxidative stress in the heart, liver and kidneys of rats generated by postmortem ischemia.

     

Selenium-Vitamin E Combination Modulates Endometrial Lipid Peroxidation and Antioxidant Enzymes in Streptozotocin-Induced Diabetic Rat

Diabetes mellitus is associated with diabetic impairment of uterine function, ultimately leading to reduced fertility. Its etiology may involve oxidative damage by reactive oxygen substances, and protection against this damage can be offered by antioxidant supplementation. In the present study, the effects of a vitamin E-plus-selenium (VESe) combination on lipid peroxidation (MDA) and the scavenging enzyme activity in the uterine endometrium of streptozotocin (STZ)-induced diabetic rats were investigated. Twenty-four female rats were equally divided into three groups as follows: group I (control); group II (diabetic); group III (diabetic + VESe), STZ + vitamin E (60?mg/kg over 1?day) + selenium-treated (Na2SeO3, 1?mg/kg over 1?day). After 4?weeks of receiving the VESe treatment, endometrium samples were taken from the uterus. Although the VESe treatment decreased the MDA and blood glucose levels in the STZ group, the observed values remained significantly higher than in the controls. Catalase, superoxide dismutase, and glutathione peroxidase activities and body weight gain were significantly (p?<?0.01) lower in STZ groups as compared to control group, whereas their activities were (p?<?0.01) increased by VESe treatment. However, there was no significant difference on body weight gain and uterine weights between control and STZ + VESe groups. In conclusion, the endometrial complications caused by oxidative stress, and the abnormal blood glucose levels in diabetic of rats, can be alleviated by strengthening the physiological antioxidative defense through the administration of vitamin E and Se.     

Neuroprotective Effects of Crocin Against Ethanol Neurotoxicity in the Animal Model of Fetal Alcohol Spectrum Disorders

Several experimental and clinical findings suggest that ethanol consumption during pregnancy activates an oxidative-inflammatory cascade followed by wide apoptotic neurodegeneration within several brain areas, including the hippocampus. Crocin can protect neurons because of its antioxidant, anti-inflammatory, and antiapoptotic effects. This study evaluated the crocin protective impact on ethanol-related neuroinflammation and neuronal apoptosis in the hippocampus of rat pups exposed to alcohol over postnatal days. Ethanol (5.25 g/kg) was administrated in milk solution (27.8 ml/kg) by intragastric intubation 2–10 days after birth. The animals received crocin (15, 30, and 45 mg/kg) 2–10 days after birth. The hippocampus-dependent memory and spatial learning were evaluated 36 days after birth using the Morris water maze task. Further, the concentrations of TNF-α and antioxidant enzymes were determined using ELISA assay to examine the antioxidant and anti-inflammatory activities. Also, immunohistochemical staining was performed to evaluate the glial fibrillary acidic protein (GFAP), Ionized calcium binding adaptor molecule 1(Iba-1), and caspase-3 expression. The administration of crocin significantly attenuated spatial memory impairment (P?<?0.01) after ethanol neurotoxicity. Also, crocin led to a significant enhancement in SOD (P?<?0.05) and GSH-PX (P?<?0.01), whereas it caused a reduction in the TNF-α and MDA concentrations compared to the ethanol group (P?<?0.01). Moreover, the hippocampal level of caspase-3 (P?<?0.01) and the number of GFAP and Iba-1-positive cells decreased in the crocin group (P?<?0.001). Crocin suppresses apoptotic signaling mediated by the oxidative-inflammatory cascade in rat pups exposed to ethanol after birth.

     

Influence of laser needle-knife on PI-3K,AKT and VEGF mRNA expression in cervical spondylotic arteriopathy model rabbits

Objective

To determine the effect of laser needle-knife on PI-3K, AKT and VEGF mRNA expression of vertebral arteries in a rabbit model of cervical spondylotic arteriopathy (CSA) and the mechanism of action involved.

Effect of Sargentodoxa cuneata total phenolic acids on focal cerebral ischemia reperfusion injury rats model

Objective

Explore the possible protective effect of Sargentodoxa cuneata total phenolic acids on cerebral ischemia reperfusion injury rats.

注射用丹酚酸A防治肝纤维化的实验研究

目的：探讨注射用丹酚酸A抗肝纤维化的作用,为丹酚酸A的临床应用提供理论依据。方法采用CCl4体外诱导肝细胞损伤,观察丹酚酸A对肝细胞活性及其细胞培养上清液ALT、AST、LDH水平和细胞裂解液中SOD活性和MDA含量的变化;另采用皮下注射CCl4诱导大鼠肝纤维化模型,观察丹酚酸A对肝纤维化大鼠血清LN、HA、SOD和MDA含量的影响以及肝脏组织病理改变情况。结果与模型对照组比,丹酚酸A高、低剂量组和Vit E组的细胞存活率显著提高（P ＜0.01）,丹酚酸A高剂量组ALT、AST和LDH活性显著降低（P ＜0.01）,丹酚酸A高剂量组和Vit E组SOD活性明显升高（P ＜0.05）,MDA含量显著降低（P ＜0.05）;体内试验发现,与模型对照组比,丹酚酸A高剂量组纤维化大鼠的血清LN和HA水平显著降低（P ＜0.05）,高、低剂量组SOD活性显著升高（P ＜0.05, P ＜0.01）,MDA含量显著降低（P ＜0.01, P ＜0.05）,并能改善肝脏病理形态。结论注射用丹酚酸A可通过抗脂质过氧化作用,起到保护肝细胞,减轻肝纤维化的作用。     

Deterioration of Bone Quality by Streptozotocin (STZ)-Induced Type 2 Diabetes Mellitus in Rats

Patients with diabetes mellitus (DM) have various skeletal disorders and bone quality can be impaired in DM leading to fractures. Wistar albino male rats (270?C300?g; n?=?16) were assigned randomly to nondiabetic and diabetic rats (single dose intravenous injection of 45?mg/kg streptozotocin). All rats in each group were perpetuated for 8?weeks, and blood glucose levels as well as body weights were measured once weekly. Biomechanical measurements were performed at the mid-diaphysis of the left femur with tensile test. Extrinsic and intrinsic properties were measured or calculated. Bone mineral density (BMD) was also evaluated and measured by dual-energy X-ray absorptiometry. Cross-sectional area of the femoral shaft was evaluated by computerized tomography. Blood glucose levels in diabetic rats were significantly increased compared to that of the nondiabetic rats, while the body and femur weights were decreased (P?<?0.05). In respect to the BMD, cross-sectional area and femur length, there were no statistically significant differences between the nondiabetic and diabetic rats (P?>?0.05). The maximum load, ultimate stress, and toughness endpoints in diabetic rats were significantly decreased compared to that of the nondiabetics (P?<?0.05). There were no statistically significant differences between the nondiabetic and diabetic rats with regard to the displacement and stiffness (P?>?0.05). Femurs of diabetic rats had less absorbed energy than that in nondiabetics (P?<?0.05). Ultimate strain was lower in diabetic rats than that in nondiabetics, while the elastic modulus was higher (P?>?0.05). The bone quality of rats is decreased by streptozotocin-induced type 2 diabetes mellitus.     

D-半乳糖致衰老模型大鼠体征和骨髓DNA含量的改变与中药干预作用

目的观察D-半乳糖致衰老模型大鼠的一般症状、皮肤状况、饮食嗜好及骨髓细胞DNA含量的变化,并探讨中药抗衰老的作用及其机制。方法大鼠每日一次皮下注射D-半乳糖,连续7周,建立衰老大鼠模型,观察衰老大鼠的一般症状和体重变化,测定其皮肤含水量、糖水消耗量和骨髓细胞DNA含量,并用抗衰老片和首乌延寿片进行干预,观察中药对衰老模型大鼠的干预作用。结果大鼠皮下注射D-半乳糖后,逐渐出现体重增长缓慢、行动迟缓、精神不振、嗜睡、被毛卷曲枯黄、光泽欠佳、尾部出现色素斑点等衰老症状,并在造模第5周出现体重下降,造模7周后,衰老大鼠的皮肤含水量和糖水消耗量明显减少（P〈0.05）,骨髓细胞的DNA含量亦明显减少（P〈0.01）;给予抗衰老片和首乌延寿片后,均可不同程度地延缓衰老症状,缓解体重的下降,显著提高皮肤的含水量和糖水消耗量（P〈0.01）,同时,明显提高骨髓细胞DNA含量（P〈0.05）。结论D-半乳糖致衰老大鼠模型的衰老体征明显,机体抗DNA损伤的能力下降,而抗衰老片和首乌延寿片等中药可明显改善衰老模型大鼠的衰老症状,其作用机制可能与提高机体修复DNA损伤的能力有关。     

Monophosphoryl Lipid A and Pam3Cys Prevent the Increase in Seizure Susceptibility and Epileptogenesis in Rats Undergoing Traumatic Brain Injury

Five percent of all epilepsy cases are attributed to traumatic brain injury (TBI), which are known as post-traumatic epilepsy (PTE). Finding preventive strategies for PTE is valuable. Remarkable feature of TBI is activation of microglia and subsequent neuroinflammation, which provokes epileptogenesis. The toll-like receptor agonists monophosphoryl lipid A (MPL) and tri-palmitoyl-S-glyceryl-cysteine (Pam3Cys) are safe, well-tolerated and effective adjuvants existing in prophylactic human vaccines. We examined the impact of early injection of MPL and Pam3Cys to rats, on the rate of kindled seizures acquisition following TBI. Rats received a single dose (1 µg/rat) of MPL or Pam3Cys through intracerebroventricular injection. 5 days later, trauma was exerted to temporo-parietal cortex of rats by controlled cortical impact device. After 24 h, traumatic rats underwent amygdala kindling. Brain level of the inflammatory cytokine tumor necrosis factor-alpha (TNF-α) was also measured in traumatic rats by immunoblotting. Compared to non-traumatic (sham-operated) rats, traumatic rats showed three times lower seizure threshold (133?±?5 µA vs. 416.3?±?16 µA, p?<?0.001); about three times less number of stimuli to become kindled (5?±?1 vs. 14?±?2, p?<?0.01); longer duration of kindled seizure parameters including entire seizure behavior, generalized seizures, and afterdischarges (p?<?0.001); and a two times increase in the TNF-α level. MPL and Pam3Cys did not change kindling rate and the seizure parameters in sham-operated rats. The MPL- and Pam3Cys-pretreated traumatic rats displayed seizure threshold, speed of kindling, and duration of kindled seizure parameters, similar to the non-traumatic rats. Pretreatment by MPL and Pam3Cys prevented the increase in TNF-α level by trauma. Given that MPL and Pam3Cys currently have clinical use as well-tolerated vaccines with reliable safety, they have the potential to be used in prevention of PTE.     

Effects of dodder total flavone on polycystic ovary syndrome rat models induced by DHEA combined HCG

AimsExplore the effects of dodder total flavone on polycystic ovary syndrome (PCOS) rat models induced by dehydroepiandrosterone (DHEA) combined human chorionic gonadotropin (HCG).MethodsExcept the blank group, the rest of the rats were injected with DHEA 6 mg/100 g on the back of the neck and 1.5 IU HCG each day, for 21 consecutive days. On the 16th day of modeling, vaginal smear was performed to select the model rats, which were randomly divided into model group, dacin-35 group, large, middle and small dose dodder total flavonoids groups, and given the medicine for three weeks. At the end of the last administration, take samples, so as to calculate the ovaries and uterus indexes, measure serum LH/FSH ratio, P, PRL and INS levels, fixed the uterus and pancreas in 10% formalin solution and stained with HE to observe the morphological changes of the organs. And measure the expression of TNF-α and IGF-l proteins in ovaries by immunohistochemistry.ResultsCompared with the blank group, ovarian and uterine indexes, serum LH/FSH ratio, serum PRL and INS levels, ovary TNF-α and IGF-l protein expression were significantly increased, and significant pathological changes were observed in the uterine and pancreatic tissues in model group (P < 0.01). While the serum P level decreased significantly (P < 0.01), Compared with the model group, the ovarian and uterine indexes, serum LH/FSH ratio, serum P, PRL and INS levels, ovary TNF-α protein expression were significantly decreased in large, middle and small dose dodder total flavonoids groups (P < 0.01); The expression of IGF-1 protein was decreased and uterus pathological changes were improved in different extents (P < 0.01 or P < 0.05), pancreas pathological changes were improved significantly (P < 0.01).ConclusionPCOS rat models was successfully replicated. Dodder total flavone can protect PCOS rats induced by DHEA combined HCG by different action pathways.     

Effect of pioglitazone on skeletal muscle lipid deposition in the insulin resistance rat model induced by high fructose diet under AMPK signaling pathway

To study the changes of lipid deposition in skeletal muscle of insulin resistance rat and the effect of pioglitazone intervention on the expression of AMPK pathway related genes in rat, a rat model of insulin resistance was induced and constructed by high fructose diet as an test group, and normal rats were used as a control group. First, the effect of pioglitazone intervention on serum lipids-related indicators and mRNA expression levels of fat-related genes in skeletal muscle in rats was investigated. Then skeletal muscle sections were made and stained with oil red O to investigate the effect of pioglitazone intervention on lipid deposition in skeletal muscle of rats. Finally, the effects of pioglitazone intervention therapy on the mRNA and protein expression of related genes in the AMPK signaling pathway in skeletal muscle tissue of rat were explored by real-time quantitative PCR (qRT-PCR) and Western-blotting technology. The results showed that the blood glucose (BG), insulin (INS), adiponectin (ADPN), free fatty acid (FFA), triglyceride (TG), and cholesterol (TC) levels in serum of the test group were higher than the control group (P < 0.05); the visceral fat weight and abdominal fat index of the test group were significantly higher than the control group (P < 0.01); after the pioglitazone intervention, all blood lipid-related indexes in the rat model were significantly lower than before the intervention (P < 0.05); skeletal muscle section staining results showed that the number of lipid droplets in skeletal muscle of rat model was significantly reduced after pioglitazone intervention; and pioglitazone intervention can significantly increase the mRNA and protein expression levels of p-ACC, GLUT7, PGC-1α, and CPT1 genes in the skeletal muscles of experimental rats (P < 0.05). Accordingly, it can be concluded that pioglitazone can play a role in treating insulin resistance by regulating the expression of related genes of AMPK, ACC, etc. in the AMPK signaling pathway.     

The effect of progesterone administration on the expression of metastasis tumor antigens (MTA1 and MTA3) in placentas of normal and dexamethasone-treated rats

Background

Dexamethasone (DEX) induces intrauterine growth restriction (IUGR) in pregnant rats. IUGR can occur due to apoptosis of trophoblasts, which is believed to be inhibited by progesterone (P4). A group of genes called MTAs play a role in proliferation and apoptosis. MTA1 upregulates trophoblasts proliferation and differentiation, while MTA3 downregulates proliferation and induces apoptosis. Hence, we hypothesized that during IUGR, placental MTA1 decreases and MTA3 increases and this is reversed by P4 treatment.

Methods

Pregnant Sprague–Dawley rats were divided into 4 groups based on daily intraperitoneal injections: control (C, saline), DEX (DEX, 0.2 mg/kg/day), DEX and P4 (DEX?+?P4, DEX: 0.2 mg/kg/day, P4: 5 mg/kg/day) and P4-treated (P4, 5 mg/kg/day) groups. Injections were started on 15 dg until the day of dissection (19 or 21 dg). Gene and protein expressions of MTA1 and MTA3 were studied in the labyrinth (LZ) and basal (BZ) zones using real-time PCR and Western blotting, respectively.

Results

DEX treatment induced 18% reduction in fetal body weight (p?<?0.001) and 30% reduction in placental weight (p?<?0.01). Maternal P4 level was also significantly lower in DEX treated groups (p?<?0.05). MTA1 expression was decreased in the LZ (gene, p?<?0.001) and BZ (protein p?<?0.01), while MTA3 protein expression was upregulated in the LZ with DEX treatment (p?<?0.001). These changes were reversed with P4 treatment.

Conclusion

The findings of the present study indicate that DEX induces IUGR through changing the expression of placental MTA1 and MTA3 antigens and P4 improved pregnancy outcome by preventing the changes in MTAs expression.

     

Crocin Inhibits Apoptosis and Astrogliosis of Hippocampus Neurons Against Methamphetamine Neurotoxicity via Antioxidant and Anti-inflammatory Mechanisms

Methamphetamine (METH) is a stimulant drug, which can cause neurotoxicity and increase the risk of neurodegenerative disorders. The mechanisms of acute METH intoxication comprise intra-neuronal events including oxidative stress, dopamine oxidation, and excitotoxicity. According to recent studies, crocin protects neurons by functioning as an anti-oxidant, anti-inflammatory, and anti-apoptotic compound. Accordingly, this study aimed to determine if crocin can protect against METH-induced neurotoxicity. Seventy-two male Wistar rats that weighed 260–300 g were randomly allocated to six groups of control (n?=?12), crocin 90 mg/kg group (n?=?12), METH (n?=?12), METH?+?crocin 30 mg/kg (n?=?12), METH?+?crocin 60 mg/kg (n?=?12), and METH?+?crocin 90 mg/kg (n?=?12). METH neurotoxicity was induced by 40 mg/kg of METH in four injections (e.g., 4?×?10 mg/kg q. 2 h, IP). Crocin was intraperitoneally (IP) injected at 30 min, 24 h, and 48 h after the final injection of METH. Seven days after METH injection, the rats’ brains were removed for biochemical assessment using the ELISA technique, and immunohistochemistry staining was used for caspase-3 and glial fibrillary acidic protein (GFAP) detection. Crocin treatment could significantly increase superoxide dismutase (P?<?0.05) and glutathione (P?<?0.01) levels and reduce malondialdehyde and TNF-α in comparison with the METH group (P?<?0.05). Moreover, crocin could significantly decline the level of caspase-3 and GFAP-positive cells in the CA1 region (P?<?0.01). According to the results, crocin exerts neuroprotective effects on METH neurotoxicity via the inhibition of apoptosis and neuroinflammation.     

D-半乳糖致衰老模型大鼠肝肾功能和自由基代谢与中药的干预作用

目的观察D-半乳糖致衰老模型大鼠血糖血脂、肝肾功能和自由基代谢的变化,探讨中药的干预作用及其抗衰老的机制。方法大鼠每日皮下注射D-半乳糖,连续造模7周,建立大鼠衰老模型,造模同时,用抗衰老片和首乌延寿片进行干预,测定试验大鼠的血糖血脂、肝肾功能和SOD、MDA、Na＋-K＋-ATPase和Ca＋＋-Mg＋＋-ATPase等自由基代谢指标。结果造模7周后,模型对照组衰老大鼠TG、BUN明显升高（P〈0.05,P〈0.01）,AST、ALP、CREA呈上升趋势（P〉0.05）,肝、肾组织SOD活性明显降低（P〈0.05）,肾组织MDA含量明显升高（P〈0.05）,肝组织Na＋-K＋-ATPase和Ca＋＋-Mg＋＋-ATPase活性均显著降低（P〈0.05,P〈0.01）;给予抗衰老片和首乌延寿片后,衰老大鼠TG、AST、BUN、CREA和UA均显著降低（P〈0.05,P〈0.01）,肝、肾组织MDA含量显著降低（P〈0.05）,SOD活性显著升高（P〈0.05,P〈0.01）,肝组织Na＋-K＋-ATPase和Ca＋＋-Mg＋＋-ATPase活性均显著升高（P〈0.01）。结论D-半乳糖致衰老大鼠模型的血脂上升、肝肾功能异常和抗脂质过氧化的能力下降;给予抗衰老片和首乌延寿片后,可有效改善衰老大鼠的糖脂代谢和肝肾功能,提高肝肾组织的抗脂质过氧化的能力,提示中药的抗衰老作用可能与其抗氧化作用有关。