Antioxidant activity of Terminalia arjuna bark extract on N-nitrosodiethylamine induced hepatocellular carcinoma in rats

Role of oxidative stress and Na⁺,K⁺-ATPase in the cytotoxicity of hexachlorocyclohexane (HCH) on Ehrlich Ascites tumor (EAT) cells has been studied. HCH caused dose dependent cell death as measured by trypan blue exclusion and lactate dehydrogenase (LDH) leakage from the cells. HCH induced oxidative stress in EAT cells which was characterized by glutathione depletion, lipid peroxidation (LPO), reactive oxygen species (ROS) production and inhibition of antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT). Protective effect of antioxidants on HCH induced oxidative stress was assessed, among the antioxidants used only quercetin inhibited HCH-induced LPO and ROS production as well as cell death whereas α -tocopherol, ascorbic acid and BHA inhibited LPO but not cell death. Inhibition of membrane bound Na⁺,K⁺-ATPase was a characteristic feature of HCH cytotoxicity in EAT cells. Experimental evidence indicates that HCH-induced cell death involves oxidative stress due to ROS production and membrane perturbation in EAT cells.     

Gastroprotective effect of Terminalia arjuna bark on diclofenac sodium induced gastric ulcer

AIM: The present study was aimed to evaluate the effect of methanolic extract of Terminalia arjuna (TA) on diclofenac sodium induced gastric ulcer in experimental rats. METHODS: Animals were induced for gastric ulcer with diclofenac sodium (DIC) (80mg/kg bodyweight in water, orally) and treated orally with TA in various doses ranging from 100mg/kg bodyweight to 500mg/kg bodyweight. The effective dose was 400mg/kg bodyweight, since this dose elicited a maximum reduction in lesion index. The gastroprotective effect of TA was assessed from volume of gastric juice, pH, free and total acidity, pepsin concentration, acid output in gastric juice, the levels of non-protein sulfhydryls (NP-SH), lipid peroxide (LPO), reduced glutathione (GSH), and activities of enzymic antioxidants--super oxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and myeloperoxidase (MPO) in gastric mucosa. The levels of DNA, protein bound carbohydrate complexes--hexose, hexoseamine, sialic acid, fucose in gastric mucosa and gastric juice and the levels of RNA in gastric mucosa were assessed. The stomach tissues were used for adherent mucus content and also for the histological examination. RESULTS: A significant reduction in lesion index was observed in ulcer induced animals treated with TA (DIC+TA) compared to ulcerated rats (DIC). A significant increase was observed in pH, NP-SH, GSH, enzymic antioxidants, protein bound carbohydrate complexes, adherent mucus content, nucleic acids with a significant decrease in volume of gastric juice, free and total acidity, pepsin concentration, acid output, LPO levels and MPO activities in DIC+TA rats compared to DIC rats. Histological studies confirmed the gastroprotective activity of TA. CONCLUSION: From the data presented in this study it could be concluded that T. arjuna acts as an gastroprotective agent probably due to its free radical scavenging activity and cytoprotective nature.     

Cardioprotective effect of lycopene in the experimental model of myocardial ischemia-reperfusion injury

The continuous advancements in cancer research have contributed to the overwhelming evidence of the presence of telomerase in primary and secondary tumours together with hsp90 and c-Myc. This review will discuss the important role of telomerase together with hsp90 and c-Myc within the initiation and progression of gliomas. Also it will review the differential expression of these genes in the different grades of gliomas and the possibility of new treatments targeting these specific genes.     

Pyruvate provides cardioprotection in the experimental model of myocardial ischemic reperfusion injury

The present study was designed to evaluate the cardioprotective potential of pyruvate and to characterize the mechanism underlying the protection. Wistar albino rats were randomly divided into three groups. Two groups were administered saline orally (sham, ischemia-reperfusion (I-R) control group) and animals of third group received pyruvate (500 mg/kg) for 4 weeks. On the 29th day, animals of the I-R control and pyruvate treated groups underwent 45 min of occlusion of the left anterior descending (LAD) coronary artery and were thereafter reperfused for 60 min. In the I-R control group, a significant cardiac necrosis, depressed mean arterial pressure (MAP) and heart rate (HR), decline in myocardial antioxidant status and elevation in lipid peroxidation were observed as compared to sham control. Pyruvate treatment restored the myocardial antioxidant status and favorably modulated the altered MAP as compared to I-R control. Furthermore, I/R-induced lipid peroxidation was significantly inhibited by pyruvate treatment. These beneficial cardioprotective effects translated into significant improvement in MAP. Histopathological examination and restored specific myocardial injury marker CK-MB isoenzyme activity further confirmed protective effects of pyruvate. In conclusion, our study has demonstrated that the beneficial effect of pyruvate likely results from improved MAP and suppression of oxidative stress.     

肾缺血预处理对心脏缺血／再灌注损伤的保护作用

目的：探讨肾缺血预处理对家兔心脏缺血／再灌注（I／R）损伤的影响及意义。方法：32只大耳白家兔随机分为假手术（SO）、心脏I／R、经典缺血预处理（CIPC）及肾缺血预处理（RIPC）4组。观察各组心肌梗塞面积、左室舒缩功能、心脏超微结构及心律失常发生率的变化。结果：CIPC、RIPC组,心肌梗塞面积、再灌性心律失常发生率较I／R组明显降低,左室舒缩功能明显恢复（P＜0.01）,心脏超微结构损伤明显减轻。结论：RIPC可诱导出与CIPC类似的心脏保护效应。     

Cardioprotection by Inula racemosa Hook in experimental model of myocardial ischemic reperfusion injury

To evaluate the cardioprotective potential of Inula racemosa in myocardial ischemic-reperfusion injury, Wistar male albino rats were randomly divided into four groups. The group I and II animals were administered saline orally {(sham, ischemia- reperfusion (I-R) control group)} and animals of group III and group IV received I. racemosa extract (100 mg/kg) for 30 days. On the 30th day, animals of I-R control and I. racemosa treated groups were underwent 45 min of ligation of left anterior descending coronary artery and were thereafter re-perfused for 60 min. In the I-R control group, a significant decrease of mean arterial pressure (MAP), heart rate (HR), contractility, (+)LVdP/dt and relaxation, (-)LVdP/dt and an increase of left ventricular end diastolic pressure (LVEDP) were observed. Subsequent to haemodynamic impairment and left ventricular contractile dysfunction, a significant decline was observed in endogenous myocardial antioxidants; superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and reduced glutathione (GSH). Increased lipid peroxidation characterized by malonaldialdehyde (MDA) formation along with depletion of cardiomyocytes specific enzymes, creatine phosphokinase-MB (CK-MB) isoenzyme and lactate dehydrogenase (LDH) in I-R control group compared to sham group revealed I-R injury of heart. However, treatment with I. racemosa significantly restored the myocardial antioxidant status evidenced by increased SOD, CAT, GPx and GSH and prevented leakage of cardio-specific enzymes; CK-MB and LDH and favorably modulated the altered MAP, HR, (+)LVdP/dt, (-)LVdP/dt and LVEDP as compared to I-R control. Furthermore, I-R induced lipid peroxidation was significantly inhibited by I. racemosa treatment. These beneficial cardioprotective effects translated into significant improvement in cardiac function. In conclusion, our study has demonstrated that the cardioprotective effect of I. racemosa likely resulted to improved antioxidant status, haemodynamic and left ventricular contractile function subsequent to suppression of oxidative stress.     

Nigella sativa attenuates myocardial ischemic reperfusion injury in rats

Myocardial ischemia–reperfusion (I/R) represents a clinically relevant problem associated with thrombolysis, angioplasty, and coronary bypass surgery. Radical oxygen species generated during early reperfusion are the primary activator of mitochondrial permeability transition pore (MPTP) opening which finally results in cardiomyocyte death. Nigella sativa (NS) has been shown to have antioxidant properties. The present study aimed to determine whether supplementation with NS can provide sufficient protection for the myocardium against I/R insult and any possible role on mitochondrial MPTP. Adult male Wistar rats were allocated into two groups: control group and NS-treated group receiving NS (800 mg/kg) orally for 12 weeks. Rats' isolated hearts were perfused in Langendorff preparation to determine the baseline heart beating rate, developed peak tension, time to peak tension, rate of tension development, half relaxation time, and myocardial flow rate. Ischemia was then induced by stopping the perfusion fluid for 30 min, followed by 30 min of reperfusion and recording post I/R cardiac functions. Hearts were then used for assessment of malondialdehyde (MDA) and nicotinamide adenine dinucleotide (NAD⁺), since the hydrolysis of mitochondrial NAD⁺ directly reflects MPTP opening in situ, and for histological examination. The NS-treated group showed enhanced post I/R contractile and vascular recovery, which was accompanied by elevated NAD⁺ and decreased MDA compared to the control group. Histological examination showed marked improvement of cardiac musculature compared to the control group. In conclusion, N. sativa afforded substantial recovery of post I/R cardiac functions probably via inhibition of MPTP opening.     

Aqueous extract of Terminalia arjuna attenuates tert‐butyl hydroperoxide–induced oxidative stress in HepG2 cell model

Arjuna (Terminalia arjuna) is a medicinal plant used in many polyherbal hepatoprotective formulations. Although widely claimed to be antioxidant, data supporting such actions of Arjuna are limited. In the present study, we have investigated the efficacy of the aqueous extract of T. arjuna (AETA) using a standard pro‐oxidant [tertiary butyl hydroperoxide (TBHP)] in HepG2 cells. Cells were incubated with AETA (5–100 µg/ml) for a range of time points (4–24 h) with or without TBHP (500 μM), and biochemical markers of oxidative stress (OS) were determined. Cells incubated with TBHP showed the significant induction of OS response in cytosol manifested as lipid hydroperoxide (76%–198%) and the generation of reactive oxygen species (60%–127%). Diminished levels of reduced glutathione (35%–60%) and total antioxidant capacity (20%–61%) suggested an altered redox state. Significant perturbations in the activities of antioxidant enzymes such as catalase (30%–56%), superoxide dismutase (25%–68%), glutathione S‐transferase (29%–67%), glutathione peroxidase (24%–68%) and glutathione reductase (38%–49%) were discernible suggesting the ongoing OS in the cells. However, cells treated with AETA (100 µg/ml) along with TBHP offered significant protection by reducing levels of lipid hydroperoxide (33%–62%) and ROS (69%) and by increasing antioxidant capacity (54%–81%) and levels of reduced glutathione (49%–82%). Further, it also enhanced the activities of endogenous antioxidant enzymes (superoxide dismutase, 60%; catalase, 35%–82%; glutathione peroxidase, 42–65 %; glutathione reductase, 48%–62%; and glutathione S‐transferase, 22%–100%). Taken together, these data suggest that Arjuna can protect against the oxidative damage induced by TBHP and may be effectively used as a hepatoprotective adjuvant to abrogate OS in vivo. Copyright © 2012 John Wiley & Sons, Ltd.     

Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning

Ischemic preconditioning (Pre-con) is an adaptive response triggered by a brief ischemia applied before a prolonged coronary occlusion. We tested the hypothesis that repetitive ischemia applied during early reperfusion, i.e., postconditioning (Post-con), is cardio-protective by attenuating reperfusion injury. In anesthetized open-chest dogs, the left anterior descending artery (LAD) was occluded for 60 min and reperfused for 3 h. In controls (n = 10), there was no intervention. In Pre-con (n = 9), the LAD was occluded for 5 min and reperfused for 10 min before the prolonged occlusion. In Post-con (n = 10), at the start of reperfusion, three cycles of 30-s reperfusion and 30-s LAD reocclusion preceded the 3 h of reperfusion. Infarct size was significantly less in the Pre-con (15 +/- 2%, P < 0.05) and Post-con (14 +/- 2%, P < 0.05) groups compared with controls (25 +/- 3%). Tissue edema (% water content) in the area at risk was comparably reduced in Pre-con (78.3 +/- 1.2, P < 0.05) and Post-con (79.7 +/- 0.6, P < 0.05) versus controls (81.5 +/- 0.4). Polymorphonuclear neutrophil (PMN) accumulation (myeloperoxidase activity, Deltaabsorbance.min-1.g tissue-1) in the area at risk myocardium was comparably reduced in Post-con (10.8 +/- 5.5, P < 0.05) and Pre-con (13.4 +/- 3.4, P < 0.05) versus controls (47.4 +/- 15.3). Basal endothelial function measured by PMN adherence to postischemic LAD endothelium (PMNs/mm2) was comparably attenuated by Post-con and Pre-con (15 +/- 0.6 and 12 +/- 0.6, P < 0.05) versus controls (37 +/- 1.5), consistent with reduced expression of P-selectin on coronary vascular endothelium in Post-con and Pre-con. Endothelial function assessed by the maximal vasodilator response of postischemic LAD to acetylcholine was significantly greater in Post-con (104 +/- 6%, P < 0.05) and Pre-con (109 +/- 5%, P < 0.05) versus controls (71 +/- 8%). Plasma malondialdehyde (microM/ml), a product of lipid peroxidation, was significantly less at 1 h of reperfusion in Post-con (2.2 +/- 0.2, P < 0.05) versus controls (3.2 +/- 0.3) associated with a decrease in superoxide levels revealed by dihydroethidium staining in the myocardial area at risk. These data suggest that Post-con is as effective as Pre-con in reducing infarct size and preserving endothelial function. Post-con may be clinically applicable in coronary interventions, coronary artery bypass surgery, organ transplantation, and peripheral revascularization where reperfusion injury is expressed.     

Protective effect of Terminalia chebula against experimental myocardial injury induced by isoproterenol

Cardioprotective effect of ethanolic extract of Terminalia chebula fruits (500 mg/kg body wt) was examined in isoproterenol (200 mg/kg body wt) induced myocardial damage in rats. In isoproterenol administered rats, the level of lipid peroxides increased significantly in the serum and heart. A significant decrease was observed in the activity of the myocardial marker enzymes with a concomitant increase in their activity in serum. Histopathological examination was carried out to confirm the myocardial necrosis. T. chebula extract pretreatment was found to ameliorate the effect of isoproterenol on lipid peroxide formation and retained the activities of the diagnostic marker enzymes.     

Fibroblast growth factors in myocardial ischemia / reperfusion injury and ischemic preconditioning

Angiogenic growth factors such as fibroblast growth factors (FGFs) are currently in clinical trials for accelerating blood vessel formation in myocardial and limb ischemic conditions. However, recent experimental evidence suggests that FGFs can also participate as endogenous cardioprotective agents. In this report, the current knowledge for FGFs implication in myocardial ischemic tolerance will be summarized. Pharmacologic preconditioning with drugs as FGFs that mimic the beneficial effects of ischemic preconditioning could lead to novel therapeutic approaches for the treatment of ischemic disorders including myocardial infarction and stroke.     

Cardioprotective activity of ethyl acetate extract of Cinnamomi Ramulus against myocardial ischemia/reperfusion injury in rats via inhibiting NLRP3 inflammasome activation and pyroptosis

BackgroundNLRP3 inflammasome activation and pyroptosis play an important role in myocardial ischemia/reperfusion injury (MI/RI). Cinnamomi ramulus (CR), is an important folk medicinal plant in China, which derived from the dried twig of Cinnamomum cassia (L.) Presl, has function of “warming and tonifying heart yang”, and traditionally utilized to treat the cold, blood-cold amenorrhea, phlegm, edema, arthralgia, and palpitations as well as improve blood circulation. The aqueous extract of C. ramulus was reported to show significant therapeutic potential for treating MI/RI. Whereas, there are no previous investigations in China or abroad has reported the cardioprotective effects and underlying mechanism of the ethyl acetate extract of C. ramulus (CREAE) and its bioactive substance cinnamic acid (CA) in triggering NLRP3 inflammasome activation and subsequent pyroptosis.PurposeThe present study aimed to assess the cardioprotective function of CREAE and CA against the MI/RI in rats and involved the underlying mechanisms.MethodsThe MI/RI model was established in male SD rats by occlusion of the left anterior descending coronary artery for 30 min followed by reperfusion for 120 min, respectively. The rats were intragastrically administered with CREAE (74 and 37 mg/kg) and CA (45 mg/kg) for 7 successive days before vascular ligation. The cardioprotective effects of CREAE and CA against myocardial injury of rats were detected by HE staining, TTC staining, echocardiograms, and myocardial enzymes detections. Serum levels of inflammatory factors, such as IL-6, IL-1β, and TNF-α, were analyzed by ELISA kits to evaluate the effects of CREAE and CA. The protein and gene expression levels of NLRP3 and the pyroptosis-related factors in heart tissue were conducted by western blot and RT-qPCR.ResultsOur results showed that CREAE and CA decrease myocardial infarct size and improve cardiac function, mitigate myocardial damage, and repress inflammatory response in rats after I/R. Mechanistically, our results revealed that CREAE and CA can dramatically suppress the activation of NLRP3 inflammasome and subsequent cardiomyocyte pyroptosis in myocardial tissues that as evidenced by downregulating the protein and gene expressions of NLRP3, ASC, IL-1β, caspase-1, gasdermin D, and N-terminal GSDMD.ConclusionsOur data indicated that CREAE and CA may attenuate MI/RI through suppression of NLRP3 inflammasome and subsequent pyroptosis-related signaling pathways.     

Cardioprotective effect of isorhamnetin against myocardial ischemia reperfusion (I/R) injury in isolated rat heart through attenuation of apoptosis

In this study, we investigated the effects of isorhamnetin on myocardial ischaemia reperfusion (I/R) injury in Langendorff-perfused rat hearts. Isorhamnetin treatment (5, 10 and 20 μg/mL) significantly alleviated cardiac morphological injury, reduced myocardial infarct size, decreased the levels of marker enzymes (LDH and CK) and improved the haemodynamic parameters, reflected by the elevated levels of the left ventricular developed pressure (LVDP), coronary flow (CF) and the maximum up/down velocity of left ventricular pressure (+dp/dt_max). Moreover, isorhamnetin reperfusion inhibited apoptosis of cardiomyocytes in the rats subjected to cardiac I/R in a dose-dependent manner concomitant with decreased protein expression of Bax and cleaved-caspase-3, as well as increased protein expression of Bcl-2. In addition, I/R-induced oxidative stress was manifestly mitigated by isorhamnetin treatment, as showed by the decreased malondialdehyde (MDA) level and increased antioxidant enzymes activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px). These results indicated that isorhamnetin exerts a protective effect against I/R-induced myocardial injury through the attenuation of apoptosis and oxidative stress.     

血红素氧合酶-1对心肌相对缺血/再灌注损伤的延迟保护作用

目的：探讨血红素氧合酶-1（HO-1）在运动预适应（EP）中对大鼠心肌相对缺血/再灌注（rI/R）损伤的延迟保护作用。方法：40只Wistar大鼠随机分为5组：正常对照组（CN）、相对缺血/再灌注组（IR）、运动预适应＋相对缺血/再灌注组（EI）、Hemin（HO-1诱导剂）＋相对缺血/再灌注组（HE）和运动预适应＋ZnPP（HO-1抑制剂）＋相对缺血/再灌注组（EZ）。测定大鼠再灌注期心率脉压乘积（PRP）、冠脉流出液MDA含量、HO-1活性等。结果：心肌HO-1活性：EI组和HE组较IR组显著升高,EZ组则显著降低。EZ组较EI组显著降低,EI组和HE组间亦有显著性差异。再灌注后60 min时间点PRP恢复率：EI组较IR组显著增高;IR组与HE组未见显著性差异,但30min时间点HE组显著增高;EZ组较EI组显著降低。冠脉流出液MDA含量：EI组、EZ组和HE组MDA含量较IR组皆显著降低;EZ组较EI组显著升高。结论：EP可以诱导HO-1合成,进而通过HO-1对24 h后发生的rI/R损伤产生延迟保护作用。     

心肌缺血预适应循环血中微囊泡对大鼠心肌I/R损伤的作用

目的：研究心肌缺血预适应（IPC）大鼠循环血中微囊泡（MVs）对大鼠在体心肌缺血/再灌注（I/R）损伤的作用及相关机制。方法：反复短暂结扎/松开大鼠冠状动脉左前降支建立大鼠IPC模型,自腹主动脉取血,超速离心法分离循环血中的IPC-MVs,并对其进行流式鉴定。建立在体大鼠心肌I/R模型,股静脉注射IPC-MVs 7 mg/kg。HE染色观察心肌形态学变化,TTC染色检测心肌梗死范围,TUNEL染色检测心肌细胞凋亡率。比色法测定血清乳酸脱氢酶（LDH）活力,分光光度法测定心肌组织caspase 3活力,Western blot法检测心肌组织Bcl-2、Bax蛋白表达水平。结果：流式细胞术检测IPC-MVs浓度为4380±745个/μl。与I/R组比较,IPC-MVs能够减轻I/R大鼠心肌组织损伤,缩小心肌梗死范围（P<0.01）,减少心肌细胞凋亡数量（P<0.01）,明显降低血清LDH活力（P<0.01）,降低心肌组织caspase 3活力（P<0.01）,升高Bcl-2蛋白表达（P<0.01）,降低Bax蛋白表达（P<0.01）,升高Bcl-2/Bax比值（P<0.01）。结论：IPC-MVs显著减轻大鼠在体心肌I/R损伤,通过上调心肌组织中Bcl-2的蛋白表达,下调Bax的蛋白表达,升高Bcl-2/Bax比值,降低caspase 3活力而发挥心肌保护作用。     

Daidzein administration in vivo reduces myocardial injury in a rat ischemia/reperfusion model by inhibiting NF-kB activation

AimsWe tested the hypothesis that daidzein may reduce myocardial damage by both inhibiting the release of cytokines and limiting the nuclear translocation of NF-kB.Main methodsMale Sprague–Dawley rats were anesthetized, and the left anterior descending coronary artery (LAD) was ligated for 25 min. Twenty-four hours after reperfusion was established, the hemodynamics and infarct size were examined.Key findingsTreatment with daidzein (10 mg/kg, i.p.) 1 h prior to the ischemia/reperfusion procedure (I/R) reduced the infarct size by 52.8% (P < 0.05). Daidzein also significantly improved I/R-induced myocardial contractile dysfunction by improving the left ventricular diastolic pressure and the positive and negative maximal values of the first derivative of the left ventricular pressure. In addition, daidzein reduced the plasma levels of TNF-α and IL-6 in I/R rats and decreased malondialdehyde levels, myeloperoxidase activity, catalase activity and neutrophil infiltration in I/R rat myocardium. Interestingly, daidzein inhibited I/R-induced myocardial apoptosis by decreasing DNA strand breaks and cleaved caspase-3 activity. Furthermore, daidzein inhibited both the nuclear translocation of NF-kB in I/R rat hearts and the H₂O₂-induced activation of NF-kB-luciferase activity in human umbilical vein endothelial cells.SignificanceThis study reveals that the administration of daidzein in vivo attenuates I/R-induced myocardial damage via inhibition of NF-kB activation, which in turn may suppress inflammatory cytokine expression.     

骨骼肌和心肌缺血后处理对兔缺血/再灌注心肌的保护作用

目的:观察骨骼肌缺血后处理(RPostC)、心肌的缺血后处理(MPostC)对缺血/再灌注心肌保护作用是否存在差异以及两者联合后作用是否叠加。方法:健康新西兰大白兔3O只,随机分为5组(n=6):缺血对照组(Con)、假手术组(sham)、心肌缺血后处理组(MPostC)和肢体缺血后处理组(RPostC)及心肌缺血后处理联合肢体缺血后处理组(MPostC+RPostC)。采用开胸结扎冠状动脉左室支45 min,再灌注120min方法制作缺血/再灌注模型,采用短暂结扎双侧髂外动脉固定部位5 min造成骨骼肌短暂缺血。以Evans蓝标记心肌缺血区范围,以TTC法检测梗死心肌范围,并分别于缺血前、后及再灌注1、2 h测定血浆磷酸肌酸激酶(CPK)活性和乳酸脱氢酶(LDH)含量。结果:和Con组相比,MPostC和RPostC组心肌梗死范围均明显降低(P<0.05);MPostC联合RPostC组心肌梗死范围与MPostC或RPostC组相比,均进一步降低(均P<0.05)。但MPostC组及RPostC组之间心肌坏死范围未见统计学差异。再灌注120 min末血浆CPK活性及LDH含量也显示相似趋势。结论:骨骼肌缺血后处理及心肌后处理对缺血/再灌注心肌均具有明显保护作用;且两者作用可以叠加;但骨骼肌和心肌后处理之间保护作用未显示统计学差异。     

白鲜皮水提物对大鼠心肌缺血再灌注损伤的保护作用

目的研究白鲜皮水提物对大鼠心肌缺血再灌注损伤的保护作用。方法 Wistar大鼠随机分为假手术组,模型组,阳性药组(地奥心血康)及白鲜皮低、中、高剂量组(白鲜皮水提物0.128、0.64、1.28 g/kg),每组6只。结扎冠状动脉左前降支制备大鼠心肌缺血再灌注损伤模型,观察给药后大鼠心电图ST段的改变,测量心肌梗死面积,观察大鼠心肌组织病理形态,检测大鼠血清CK,SOD活性、MDA含量。结果白鲜皮中、高剂量组给药后能明显减少心肌梗死面积,明显降低缺血30 min和再灌注120 min时ST段的抬高,并能降低大鼠血清中MDA含量,升高SOD活性,减少因缺血导致的心肌组织病理损害。结论白鲜皮水提物对大鼠心肌缺血再灌注损伤具有保护作用,其作用机制可能与保护心肌细胞功能、提高心肌抗氧化能力、清除氧自由基有关。     

Cardioprotective effect of aqueous extract of Embelia ribes Burm fruits against isoproterenol-induced myocardial infarction in albino rats

In the present study, cardioprotective effect of aqueous extract of fruits of Embelia ribes Burm (ER) was evaluated in a rat model having acute myocardial infarction, induced by isoproterenol (5.25 and 8.5 mg/kg, sc, for two consecutive days). Aqueous ER extract (100 mg/kg) pretreatment orally for 40 days in isoproterenol (ISO)-treated rats significantly decreased the heart rate, systolic blood pressure, increased levels of serum lactate dehydrogenase, serum creatine kinase and myocardial lipid peroxides and significantly increased the myocardial endogenous antioxidants (glutathione, superoxide dismutase and catalase) levels. The results of biochemical observations in serum and heart tissues were supplemented by histopathological examination of rat's heart sections to confirm the myocardial injury. The results were comparable to that of gliclazide treated group. The present results provide evidence for the first time, that aqueous ER extract pretreatment ameliorated myocardial injury and enhanced the antioxidant defense against ISO-induced myocardial infarction in rats and exhibited cardioprotective property.