OBJECTIVE: To observe the effect of recipes replenishing qi and activating blood on cell proliferation and apoptosis in the liver of natural aging rats. METHODS: Natural aging rats were under administration of recipes replenishing qi or activating blood for 4 months. The liver of the rats was prepared into cell suspension for determination of cell proliferation and apoptosis with PI-staining and flow cytometer. RESULTS: (1) Compared with those of the young rats, the cells in G(0)-G1 phase in the liver tissue of aging rats were increased (P< 0.01), and apoptosis cells were increased (P< 0.01), while the cells in S and G2-M phases were decreased (P< 0.01). (2) Compared with those of the aging rats, the cells in G(0)-G1 phase in the liver tissue of aging rats administered recipes replenishing qi or activating blood were decreased (P< 0.01), and it was more obvious in activating blood group than in replenishing qi group (P< 0.01); the cells in S and G2-M phases were increased (P< 0.01) and there was no significant difference between the activating blood group and the replenishing qi group (P> 0.05). (3) The apoptosis cells in replenishing qi or activating blood group were decreased significantly (P< 0.01), and the effect of replenishing qi was better than that of activating blood (P< 0.01). CONCLUSION: (1) Cell proliferation is decreased and apoptosis is increased in the liver tissue of natural aging rats. (2) Recipes replenishing qi or activating blood can accelerate cell proliferation in the liver tissue of natural aging rats, and the effect of activating blood was slightly stronger than that of replenishing qi. (3) Recipes replenishing qi or activating blood can inhibit cell apoptosis in the liver tissue of natural aging rats, and the effect of replenishing qi was better than that of activating blood.

Object To study the effect and mechanism of heart beneficial recipe (HBR) on ? amyloid induced neuronal apoptosis Methods In order to establish neurotoxic model, the primary cultured rat hippocampal neurons were treated with 25 ?mol/L aggregated ? amyloid fragment 1 42 (A? 1 42) Neuronal survival was assessed by viable counting after double stained with fluorescein diacetate (FDA) and propidium iodide (PI) Apoptosis of neurons was determined by Hoechst 33258 staining and terminal transferase deoxyuridine nick end labeling (TUNEL) staining The protein expression of Caspase 3 was examined by immunocytochemical SABC method The transcription of mRNAs related to bcl 2, bax, c jun and c fos gene were observed by Northern Blot or RT PCR method Results In the A? 1 42 treated neurons, the number of viable cell was decreased Hoechst 33258 staining showed condensation of nuclear chromatin and nuclear fragmentation TUNEL staining revealed that the number of positive neuron was increased The expression of Caspase 3 protein was elevated The expression of bcl 2 mRNA was decreased, but bax and c jun mRNA were inereased After HBR treatment, the above indexes were improved Conclusion HBR could regulate the expression of apoptosis associated gene and Caspase 3, attenuate the neurotoxic action of A? 1 42 and improve neuronal viability via suppressing apoptotic process

Oxidative stress has been implicated in brain injury after ischemia, which is a complex cascade. These oxidants produced by oxidative stress are directly involved in oxidative damage with cellular macromolecules such as lipids, proteins and nucleic acids, which lead to cell death. Oxidants are also mediators in signaling involving mitochondria pathway, DNA repair enzymes, and transcription factor that may lead to apoptosis after cerebral ischemia. Antioxidangt enzymes (such as superoxide dismutase,etc) provide useful tools in dissecting the events involving oxidative stress in signaling and damage in ischemic brain injury. This review focuses on the mechanisms of oxidative stress during brain ischemia.

AIM: To investigate the changes of cardiac function, oxidative stress and apoptosis in myocardium of rat model of heart failure induced by adriamycin (ADR). METHODS: At the end of the study, we observed content of malondialdehyde (MDA), activity of superoxide dismutase (SOD) and apoptosis. Expression of P53 protein and p53 mRNA were measured with immunohistochemical method and RT-PCR, respectively. RESULTS: Our data showed that content of MDA increased, activity of SOD decreased and apoptosis in myocardium happened while cardiac function decreased after ADR treatment. p53 gene expression and P53 protein obviously increased in heart failure group. CONCLUSION: There were oxidative stress and apoptosis occurred significantly in a model of heart failure induced by ADR. p53 gene might play an important role in the apoptosis. Correlation analyses suggested that apoptosis in myocardium is related to oxidative stress in ADR-induced heart failure.

AIM: The present study was designed to determine whether Sini decoction (SND), a traditional Chinese medicine, induces delayed preconditioning-like effect in rat heart and the possible mechanism by which ischemia myocardium is protected. METHODS: Sprage-Dawleyt rats underwent three 5 min episodes of preconditioning ischemia 24 h prior to the global ischemia and reperfusion in ischemic preconditioning/second window of protection (IPC/SWOP) group or were pretreated with Sini decoction (5 mL?kg -1 ?d -1 for 3 days, the last treatment 24 h before global ischemia and reperfusion) in SND group. Myocardial infarct size, CK, LDH and NO were examined. p38 MAPK and PKC were determined by immunohistochemisty. RESULTS: Myocardial infarct size was significantly decreased, CK and LDH were decreased in the serum, NO 2 -/NO 3 - was increased in myocardial tissue in SND group as well as in IPC/SWOP group (there was no difference between the two groups). The expression of p38 MAPK and PKC were upregulated in myocardial tissue in SND and IPC/SWOP groups. CONCLUSION: These results suggest that Sini decoction induces delayed preconditioning-like effect in the rat heart, possibly via inducing p38 MAPK activation.

AIM: To investigate the effect of Sini decoction (SND)on the ultrastructure of small intestinal epithelial cells in rats with intestinal ischemia-reperfusion. METHODS: Thirty-two Sprague-Dawley rats of both sexes were randomly divided into 4 groups: (1) Control group in which sham operation was performed; (2) Model group in which intestinal I/R was produced by clamping super mesenteric artery(SMA) for 1 hour and declamping SMA for 3 hours; (3) SND1 group in which SD (0.6 g/200 g rat) was given via stomach tube 3 d before intestinal I/R; (4) SND2 group in which SD (1.2 g/200 g rat)was given via stomach tube 3 d before intestinal I/R. A strip of small intestine was taken from distal end of ileum for electron microscopic examination. The two-dimensional structural parameters and three-dimensional structural parameters of mitochondria were calculated. RESULTS: (1)Morphological changes of small intestine: In control group, epithelial cells were orderly arranged, with normal mitochondria and intestinal villi. In model group, the gaps between epithelial cells widened. There were a lot of apoptotic cells. Microvilli were short and swelled. Mitochondria were swelled obviously with broken ridges. Endoplasmatic reticulum was severely dilated. In SND1 and SND2 groups, microvilli and epithelial cells were orderly arranged relatively, mitochondria was slightly swelled. (2) Structural parameters of mitochondria: In model group, there were the least mitochondria and the swelling of mitochondria was severe. In SND1 and SND2 groups, the mitochondria was more than that of model group and the swelling were slight. CONCLUSION: Sini decoction can protect small intestine from ischemia-reperfusion injury without dose-dependent effect.

OBJECTIVE: To introduce the method of analyzing repeated data measured by water maze with SPSS 11.0, and offer a reference statistical method to clinical and basic medicine researchers who take the design of repeated measures. METHODS: Using repeated measures and multivariate analysis of variance (ANOVA) process of the general linear model in SPSS and giving comparison among different groups and different measure time pairwise. RESULTS: Firstly, Mauchly's test of sphericity should be used to judge whether there were relations among the repeatedly measured data. If any (P

AIM: To detect the effect of Sini decoction on glutathione S-transferase (GST) mRNA expression in the ischemic myocardium. METHODS: Kunming mice were randomly divided into control group, ischemic group and Sini decoction group. Total RNA was extracted from the myocardium of mice in each group. The effect of Sini decoction on the expression of GST gene was detected by RT-PCR. RESULTS: The expression of GST mRNA in Sini decoction group was significantly up-regulated compared with the ischemic group and control group. CONCLUSION: Sini decoction can promote the expression of GST gene, which may be related to its protective effect on ischemic myocardium.

AIM: To screen the differentially expressed genes among normal, ischemic and Sini decoction-treated myocardium using DNA microarray.METHODS: Kunming mice were randomly divided into control group, ischemic group and Sini decoction group. Total RNA was extracted from myocardium of each group. cDNA microarray chips containing 2 304 cDNAs were used to investigate the gene expression pattern of each group. RESULTS: Up-and down-regulated genes were 33 and 70 in ischemic group vs control group, respectively. Up-and down-regulated genes were 23 and 52 respectively in Sini decoction group vs ischemic group. CONCLUSIONS: The analysis of gene expression pattern of ischemic myocardium based on cDNA microarray can realize high-throughput screening of the genes. Further analysis of those obtained genes information will be helpful to understand the molecular mechanism of myocardial ischemia and the therapeutic mechanism of Sini decoction.

AIM: The work was designed to explore protective effects of a traditional Chinese medicine-sini decoction (SD) on liver in hemorrhagic shock and its mechanism relating to oxygen free radical and nitric oxide. METHODS: Anesthetized Wistar rats were subjected to a hemorrhagic shock protocol for 60 min followed by intravenous injection with normal sodium chloride solution or SD solution. Superoxide dismutase (SOD), malondialdehyde (MDA) and nitric oxide (NO) in liver were examined. The inducible nitric oxide synthase (iNOS) was determined immunohistochemically. RT-polymerase chain reaction (RT-PCR)was used to assay the mRNA, which were corresponding to eNOS (endothelial nitric oxide synthase) and iNOS. RESULTS: The activity of SOD decreased, while the concentration of MDA increased in liver during hemorrhagic shock. SD enhanced SOD activity and inhibited a increase in MDA level in liver ( P