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Objective: To investigate the effects of Guipitang (GPT) on myocardial ischemic (MI) injury of rats. Methods: Forty male SD rats were randomly divided into five groups as control, model, GPT low-dose and high-dose groups (7.52, 15.04 g/kg), and positive-drug trimetazidine group (2 mg/kg). Rat myocardial ischemia model was induced by feeding high fat forage and intraperitoneal injection of isoprenaline (ISO). After 15 days intragastric administration, rats were injected with ISO once a day for 3 days again. Subsequently, Electrocardiograph (ECG) was examined, serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and glucose (GLU) were detected using an automatic biochemical analyzer. The histopathological alterations of heart were assessed using HE and Masson staining. The protein expressions of Collagen I and Collagen III in heart were evaluated by Western blot. Results: Compared with control group, the electrocardiogram S-T segment of model rats moved down, the serum levels of TC, AST, CK, LDH and GLU in model group were increased significantly ( P ＜0.05), the expressions of collagen I and collagen III in heart were increased ( P ＜0.05), and the hearts were damaged severely. However, no significant changes of TG, HDL-C, LDL-C and ALT were observed ( P ＞0.05). Compared with the model group, the high and low dose groups of GPT and trimetazidine could inhibit the descent of S-T segment, reduced serum TC, AST, CK, LDH and GLU levels ( P ＜0.05), and decreased collagen III expression in heart ( P ＜0.05), and alleviated myocardial pathological damage as well. The high dose group of GPT could decrease the protein expression of collagen I. Conclusion: GPT could improve heart function and alleviate the injury of myocardial ischemia, especially the high lose.

The study was aimed to investigate the effect of alpha-lipoic acid (ALA) on human umbilical vein endothelial cells (HUVECs) injury induced by hydrogen peroxide (H 2 O 2 ) and to explore its possible mechanisms. We established the H 2 O 2 -induced HUVECs injury model and the ALA treatment groups in which HUVECs were co-incubated with H 2 O 2 (250 μmol/L) and different final concentrations of ALA (100,200,400 μmol/L) for 48 h. Cell survival rate assay and LDH activity assay were carried out. The levels of related proteins were performed by Western Blot. We observed that H 2 O 2 administration resulted in an increase in the LDH activity and a decrease in cell survival rate. The expression levels of Nox4, Bax, NF-κB p65, Caspase-9, Caspase-3, iNOS, VCAM-1 and ICAM-1 were up-regulated, while the expression level of Bcl-2 was down-regulated. All these factors were significantly improved by ALA treatment. In brief, ALA treatment ameliorates H 2 O 2 -induced HUVECs damage by inhibiting inflammation and oxidative stress.

Objective: To observe the influence of electroacupuncture (EA) intervention on hippocampal glutamate (Glu) and Ca 2+ contents, and expression of Glu-N-methyl-D-aspartic acid receptor(NMDAR) and the learning-memory ability in vascular dementia (VD) rats, so as to reveal its mechanisms underlying improvement of VD., Methods: SD rats were rando-mized into sham operation (sham) group ( n =9), model group ( n =11) and EA groups ( n =10). The VD model was established by repeated bilateral common carotid arteries occlusion and reperfusion plus intraperitoneal injection of sodium nitroprusside. EA (2 Hz, 2 mA) was applied to "Baihui" (GV 20)-"Housanli" (ST 36) and "Geshu" (BL 17)-"Dazhui" (GV 14) for 10 min, once a day for 15 consecutive days. The neurological function was assessed by using stroke index (0-10 points) and neurological deficit scaling(0-10 points). The learning-memory ability was evaluated by using step-down tests. The contents of Glu and Ca 2+ in the right hippocampal tissue were determined by using aspectrophotometer and the expression of NMDAR protein in the right hippocampus was detected by immunoblotting., Results: Compared with the sham group, the stroke index and neurological deficit scores, and the reaction latency and the error times of step-down tests, as well as the contents of Glu and Ca 2+ and the expression level of NMDAR in the right hippocampus were significantly increased in the model group ( P <0.05, P <0.01), while the step-through latency was considerably decreased ( P <0.01), suggesting a neurological disorder and a cognitive decline. After EA intervention, the reaction latency and error times of step-down tests, the contents of Glu and Ca 2+ and the expression level of NMDAR in the right hippocampus were significantly down-regulated, and the step-through latency was notably increased in comparison with the model group ( P <0.01)., Conclusions: EA intervention is able to improve the cognitive ability of VD rats, which may be associated with its effects in reducing the excitatory neurotoxicity of hippocampal Glu-NMDAR and lowering cellular Ca 2+ load to resist neuronal injury.

Objective: To explore mechanisms of acupuncture for reducing of body weight., Methods: The rat obesity model was developed by subcutaneous injection of sodium glutamate solution, and the experimental rats were divided into a blank control group, a model group, an electroacupuncture group and a sibutramine group; blood TC, TG, HDL-C, LDL-C contents and lipoprotein lipase (LPL) activity, and serum leptin and insulin levels were determined., Results: The body weight and Lee's index, and TG, TC and LDL-C contents in the electroacupuncture group decreased significantly as compared with those in the model group (all P<0.01), the actions in the electroacupuncture group being superior to those in the sibutramine group; the HDL-C contents in both the electroacupuncture and the sibutramine groups were higher than that of the model group (P<0.01) with no significant difference between the electroacupuncture group and the sibutramine group; LPL activity in the electroacupuncture group increased significantly as compared with that in the model group (P<0.01); serum leptin and insulin levels in both the electroacupuncture group and the sibutramine group were lower than that in the model group (P<0.05, P<0.01), with no significant difference between the electroacupuncture group and the sibutramine group in the effect on insulin content, and the decrease of leptin level in the electroacupuncture group was more as compared with the sibutramine group (P<0.01)., Conclusion: Electroacupuncture can improve the status of high blood lipids, increase lipoprotein lipase activity, and regulate serum leptin and insulin levels in the obestic rat.

Aim: To study the effect of taurine (Tau) on rabbit cardiomyocyte apoptosis during ischemia/reperfusion (I/R) injury., Methods: Rabbit heart I/R injury was induced by occluding the left anterior descending coronary artery for 45 min and reperfusion for 180 min. taurine (200 mg/kg) was intravenously injected 5 min before heart ischemia. Cardiomyocyte apoptosis was measured by using terminal deoxynucleotidyl transferase--mediated dUTP nick end labeling method (TUNEL), flow cytometry (FCM) and DNA agarose gel electrophoresis., Results: DNA ladder pattern of DNA in myocardium was revealed by agarose gel electrophoresis in I/R group while was not found in Tau + I/R group. Apoptotic cardiomyocytes were sparse within ischemic myocardium at risk in Tau + I/ R group as compared with that in I/R group (TUNEL stain). Apoptosis rate in ischemic myocardium from I/R and Tau + I/R groups detected by flow cytometry was 17.66% +/- 1.54% and 4.86% +/- 1.23%, respectively. Fas and Bax protein expressions in ischemic myocardium of I/R group were higher than that in nonischemic myocardium group (P < 0.01), Bcl-2/Bax ratio in I/R group was lower than that in nonischemic myocardium (P < 0.01); while in Tau + I/R group, Fas and Bax protein expressions were lower than that in I/R group (P < 0.01), the Bcl-2/Bax ratio was higher than that in I/R group (P < 0.01)., Conclusion: Taurine reduced apoptosis of myocytes in I/R rabbit heart; its mechanism may involve Fas, Bax and Bcl-2 proteins expression.