Objective To observe the therapeutically effect of kangnao liquid on Pi3k mRNA and Aktm RNA ex-pressions in rats with focal cerebral ischemia-reperfusion (I/R) injury. Methods 180 male SD rats were randomly divided into 6 groups:sham operated group, model group, three kangnao liquid groups (high-dose, medium-dose and low-dose) and nimodipine group. Rats in kangnao liquid groups were administrated with kangnao liquid of 24 g/(kg · d), 12 g/(kg · d) and 6 g/(kg · d), orally once a day. Rats in nimodipine group were given nimodipine 1 mg/(kg · d). Rats in model group and sham group were treated with the same volume of distilled water for 7 days. The animal model of middle cerebral artery occlusion (MCAO) was established by a monofilament method from right internal carotid artery. The neurological evaluation was per-formed 24 h after reperfusion. The in situ hybridization was used to investigate the expression levels of Pi3k mRNA and Akt mRNA in rats on 12 h, 24 h, 48 h, 72 h and 168 h after ischemia for 2 h. Results Compared with model group, neurological functions were improved significantly in kangnao liquid groups. The expression levels of Pi3k mRNA and Akt mRNA were al-so significantly higher in kangnao liquid groups than those of model group. The expression levels of Pi3k mRNA and Akt mRNA were significantly higher in nimodipine group than those of model group, but which were lower compared with those of high-dose and medium-dose kangnao liquid groups. Conclusion Kangnao liquid can protect nerve cells by enhancing the expressions of Pi3k mRNA and Akt mRNA in rats with cerebral ischemia-reprefusion injury.

Objective To explore the expression and significance of uncoupling protein (UCP)2in rats models of acute liver failure (ALF). Methods Thirty-six healthy male SD rats were randomly divided into normal control group and model group, and the model group was divided into 5 subgroups:6, 12, 24, 36 and 48 hours sub groups with 6 rats in each sub group. The rat model of ALF was established by intraperitoneal injections of D-galactosamine (D-Gal) and lipopolysaccharide (LPS).Sections of liver tissue were stained with hematoxylin and eosin and observed under optical microscope.UCP2 and UCP2 mRNA in rat liver were determined at different time points with immunohistochemical method and reverse transcription-polymerase chain reaction ( RT-PCR ),respectively. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and malondialdehyde (MDA) concentration in the liver tissues were analyzed at the same time points.Comparisons among all the experimental groups were done by SNK test. Results Infiltration of inflammatory cells and necrosis of hepatic cells were marked in model group,and ALT, AST and MDA in model group were significantly higher than those in control group [(24. 0 ± 2. 0) U/L, (82. 3±16. 9) U/L, (2. 55±0. 22)μmol/g] at all time points. And they reached a peak at 24 h [(8346. 7±1363. 1) U/L, (9766. 7±1274. 1) U/L, (8. 34±1. 13) μmol/g; all P<0. 05]. UCP2 and UCP2 mRNA expressed scarcely in the liver tissues of control group, while increased markedly from 6 to 48 hours after D-Gal/LPS challenge in model group (P<0. 05). They both reached a peak at 24 h. And the discrepancy between consecutive experimental group had statistical significance ( P < 0. 05).Conclusions The rat model of ALF was established successfully by intraperitoneal injections of D-gal and LPS. The expression levels of UCP2 mRNA and UCP2 are consistent with the extent of liver injury and the level of oxidative stress in the rat model of ALF.

Objective To understand HIV incidence in community residents and epidemiological characteristics of newly detected HIV infection cases in Dali,Yunnan province.Methods A cohort study was conducted among 146720 community residents who were tested to be HIV negative during 2010-2011,they were followed-up from June 1,2014 to May 31,2015.Results A total of 136356 community residents received follow up (92.9％).The follow-up time was 0.23-5.40 years (medium:3.43 years),cumulatively 459675 person years,and 78 people were found to be HIV positive.The incidence rate of HIV infection was 0.170/1000 person years.The incidence rate was 0.037/1000 person years in age group 15-29 years,0.288/1000 person years in age group 30-44 years,0.210/1000 person years in age group 45-59 years,0.204/1000 person years in age ≥60 years;0.213/1 000 person years in males,0.130/1000 person years in females;0.248/1000 person years inHan ethnic group,0.149/1000 person years in Minorities;0.194/1000 in people with education level ≤junior middle school,0.046/1000 person years in people with education level ＞ junior middle school;0.070/1000 person years in the unmarried,0.194/1000 person years in the married and 0.425/1000person years in the divorced/widowed.Cox proportional hazards regression analysis showed that being male (HR=l.731),aged 30-44 years (HR=13.158),aged 45-59 years (HR=10.329),aged ≥60years (HR=8.291),unmarried (HR=3.162) and divorced/widowed (HR=2.689) were the risk factors for HIV infection,while the education level ＞ junior middle school (HR=0.132) was the protective factor for HIV infection.Conclusions By medium 3.43 years follow up,the cohort study showed that incidence rate HIV infection was 0.170/1000 person years in the community residents in Dali.Male,middle aged and old people,people with low education level,the unmarried and the divorced/widowed had relatively higher risk to be infected with HIV,Close attention should be paid to the prevention and control of AIDS in these populations.

OBJECTIVE: To investigate the effects of sera from rats fed with tablets (HGT) on endoplasmic reticulum (ER) stress in a steatotic hepatocyte model of free fatty acids (FFAs)-induced nonalcoholic fatty liver disease (NAFLD) and explore the possible mechanism. METHODS: FFAs prepared by mixing oleic acid and palmitic acid at the ratio of 2:1. HepG2 cells were treated with the sera from rats fed with low-, moderate-or high-dose HGT (HGT sera) or sera of rats fed with fenofibrate (fenofibrate sera), followed by treatment with 1 mmol/L FFAs for 24 h to induce hepatic steatosis. Oil red O staining was used to observe the distribution of lipid droplets in the cells. The biochemical parameters including triglyceride (TG), lactated hydrogenase (LDH), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured using a commercial kit. The morphological changes of the ER in the cells were observed using transmission electron microscopy. The protein/mRNA expressions of ER stress-related signal molecules including GRP78, PERK, p-PERK, ATF6, ATF4, CASPASE-12, CHOP, XBP-1, PKC, and p-PKC-δ were detected using Western blotting and/or quantitative real-time PCR (qRT-PCR). The changes in the protein expressions of GRP78, p-PERK, CASPASE-12 and CHOP were also detected in cells with transient transfection of PKC-δ siRNA for PKC-δ knockdown. RESULTS: Compared with the control cells, the cells treated with FFAs showed significantly increased levels of TG, AST, and ALT ( < 0.05). Compared with FFAs-treated cells, the cells pretreated with HGT sera or fenofibrate sera all showed significantly decreased TG, AST and ALT levels ( < 0.05), reduced accumulation of the lipid droplets ( < 0.05), and lowered protein or mRNA expression levels of GRP78, p-PERK, ATF6, ATF4, CHOP, CASPASE-12, XBP-1 and p-PKC-δ ( < 0.05). PKC-δ knockdown caused significantly reduced protein expressions of GRP78, p-PERK, CASPASE-12 and CHOP in the cells with FFA-induced hepatic steatosis ( < 0.001); treatment with high-dose HGT serum more significantly reduced the expressions of GRP78 ( < 0.001) and P-PERK ( < 0.01) in FFAs-induced cells with PKC-δ knockdown. CONCLUSIONS HGT serum can effectively prevent FFAs-induced steatosis in HepG2 cells by alleviating ER stress, in which PKC-δ may act as an important target.
Alanine Transaminase ; blood ; Animals ; Aspartate Aminotransferases ; blood ; Disease Models, Animal ; Drugs, Chinese Herbal ; administration & dosage ; Endoplasmic Reticulum ; ultrastructure ; Endoplasmic Reticulum Stress ; drug effects ; Fatty Acids, Nonesterified ; Fenofibrate ; administration & dosage ; Hep G2 Cells ; Humans ; Hypolipidemic Agents ; administration & dosage ; Microscopy, Electron, Transmission ; Non-alcoholic Fatty Liver Disease ; blood ; etiology ; prevention & control ; RNA, Messenger ; blood ; Rats ; Serum ; Tablets ; Triglycerides ; blood