3 Traditional Chinese Medicine

3 Traditional Chinese Medicine

2015140 The mechanism of Tenuigenin for eliminating waste product accumulation in cerebral neurons of Alzheimer's disease rats via ubiquitin-proteasome pathway.CHEN Qin（陳勤），et al.Sch Life Sci，Anhui Univ，Hefei 230601.Chin J Integr Trad&West Med 2015；35（3）：327-332.

Objective To explore the scavenging action of tenuigenin（TEN）on intracerebral amyloid β protein （Aβ）aggregation and the abnormal phosphorylated Tau protein and its mechanism in Alzheimer's disease（AD）rats'brain.Methods Aβ1-40was injected into the right CA1 region hippocampus to establish the AD model. Successfully，modeled rats were divided into the model group，the low，middle，high TEN group.Rats were administered with TEN（18.5，37.0，74.0 mg/kg）by gastrogavage.Besides，a sham-operation group was set up. Expression levels of Aβ1-40and Tau p-Ser262were detected by immunohistochemistry.Expression levels of ubiquitin（Ub）and Ub-protein ligase E3were measured by Western blotting.The content of 26S proteasome was detected by ELISA.Results Immunohistochemical results showed that the number of Aβ and Tau p-Ser262positively reacted neurons significantly increased in model group，when compared with the sham-operation group（P＜0.01）.Results of Western blot showed expression levels of ubiquitinated protein were up-regulated and those of Ub-protein ligase E3were down-regulated in the model group（P＜0.01）.ELISA results showed that the content of 26S proteasome significantly decreased in AD rats' brain（P＜0.01）.Compared with the model group，expression levels of Aβ1-40，Tau p-Ser22，and Ub significantly decreased；expression levels o Ub-protein ligase E3apparently increased；the content of 26s proteasome significantly increased in each TEN treatment group （P＜0.05，P＜0.01）.Best effect was shown in 37.0 mg/kg and 74.0 mg/kg TEN groups.Conclusion Ub proteasome pathway（UPP）participated in the occurrence of AD.TEN could obviously reduce intracerebral Aβ1-40accumulation and abnormal Tau phosphorylation.

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2015141 Intervention of berberine on lipid deposition in liver cells of non-alcoholic fatty liver disease rats induced by high fat diet.HAN Li（韓莉），et al. 1st Affil Hosp，Jinan Univ，Guangzhou 510632.Chin J Integr Trad&West Med 2015；35（3）：314-319.

Objective To explore the effect of berberine on lipid metabolism disorder and lipid deposition in liver cells of non-alcoholic fatty liver disease（NAFLD）rats induced by high fat diet.Methods After one week adaptable feeding，45 SPF level male SD rats were randomly divided into 3 groups，the normal control group，the model group，and the berberine group，15 in each group.Except those in the normal control group，all rats were fed with high fat diet to prepare NAFLD model.As for rats in the berberine group，Berberine Hydrochloride was administered by gastrogavage.HE Staining the all red O staining were performed to identify the model after 8 weeks.Hepatocytes were isolated，and their activities and purities were tested by Typan blue staining and flow cytometry（FCM）.Serum levels of TC，TG，HDL-C，and LDL-C were detected using automatic biochemical analyzer.mRNA expression levels of LXRα and FAS in liver cells were analyzed by Real-time quantitative polymerase chain reaction（PCR）.Protein levels of LXRα and FAS in liver cells were examined by Western blot. Results The NAFLD rat model was successfully established by hight fat diet.The yields of purified liver cells in each rat were（6.0-7.5）×108.The viability of isolated liver cells with purity over 90%（tested by FCM analysis）was higher than 95%.Compared with the normal control group，the expression of LXRα and FAS at mRNA and protein levels was higher in the model group （P＜0.01）.Compared with the model group，the expression of LXRα and FAS at mRNA and protein levels were obviously down-regulated in the berberine group （P＜0.01）.Conclusion LXRα/FAS signaling pathway was one of imporant signaling pathways of NAFLD lipid metabolism disorders.Berberine could recover hepatocyte fatty deposits in NAFLD rats by adjusting the LXR/ FAS signaling pathway of hepatocytes，which might be one of important mechanisms for fighting against NAFLD.

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2015142 Treatment of acute cholestatic hepatitis by compound Yindan decoction：a clinical observation. SUN Fengxia（孫鳳霞），et al.Dept Liver Dis，Beijing Ditan Hosp，Capital Med Univ，Beijing 100015.Chin J Integr Trad&West Med 2015；35（3）：310-313.

Objective To observe the clinical efficacy of comprehensive Western medical treatment plus Compound Yindan Decoction（CYD）in treatment of acute cholestatic hepatitis（ACH）.Methods Using randomized controlled study，60 ACH patients in line with inclusive criteria were randomly assigned to the treatment group（treated by comprehensive Western medical treatment plus CYD）and the control group（treated by comprehensive Western medical treatment alone），30 in each group. Scores for symptoms and levels of liver functions［total bilirubin（TBIL），direct bilirubin（DBIL），alkaline phosphatase（ALP），glutamyl transpeptidase（GGT），total biliary acid（TBA）］were observed before and after treatment.Results Compared with those before treatment in the same group，total scores for symptoms decreased in the treatment group and the control group at the end of the 1st and the 4th week after treatment（all P＜0.05）. Compared with the control group， total scores for symp-toms decreased in the treatment group at the end of the 1st week（P＜0.05）.Compared with those before treatment，serum levels of TBIL，DBIL，ALP，GGT，and TBA all decreased in the two groups at the end of the 4th week after treatment（P＜0.01）.Compared with the control group，serum levels of TBIL，DBIL，ALP，GGT，and TBA all decreased in the treatment group at the end of the 1st and the 2nd week after treatment（P＜0.05）. Compared with the control group，the average time for TBIL and DBIL decreasing to the level less than five times the normal value was significantly shorter in the treatment group（P＜0.05）.Conclusion CYD could significantly improve clinical symptoms of ACH patients，decrease serum levels of TBIL and DBIL，reduce serum levels of ALP，GGT，and TBA，obviously improve cholestasis，and promote the recover.

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2015143 Treatment of early and mid-term primary biliary cirrhosis by Qingying Huoxue decoction combined ursodeoxycholic acid：a clinical observation. FU Decai（付德才），et al.Dept Integr Med Hepatol，No.5 People's Hosp，Jiangnan Univ，Nanjing 214005. Chin J Integr Trad&West 2015；35（3）：290-293.

Objective To observe the clinical efficacy by Qingying Huoxue Decoction（QHD）combined ursodeoxycholic acid（UDCA）in treating patients with early and mid-term primary biliary cirrhosis（PBC）.Methods Totally 78 patients were randomly assigned to the treatment group and the control group，39 in each group.All patients received basic treatment and took UDCA（at the daily dose of 13-15 mg/kg）.Patients in the treatment group took QHD，one dose per day.The treatment course for all was 6 weeks.Clinical efficacy，gamma-glutamyl transferase （γ-GGT），alkaline phospatase（ALP），TBIL，alanine aminotransferase（ALT），and aspartate transaminase （AST）were observed before and after treatment.Results Totally 21（53.8%）patients obtained complete response in the treatment group，with statistical difference when compared with that of the control group（11 cases，30.8%）.Levels of GGT，ALP，ALT，AST，and TBIL decreased in the two groups after treatment（P＜0.01）. Levels of ALP，GGT，and TBIL were obviously lower in the treatment group than in the control group（P＜0.05）.Conclusion QHD combined UDCA in treating early and mid-term PBC patients was superior to the effect of using UDCA alone.It also could improve patients'liver function.

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2015144 Treating ischemic stroke patients of deficiency of Qi and Yin syndrome and static blood obstructingcollateralssyndromebyYangyinYiqi Huoxue recipe：a clinical study of therapeutic effect. WAN Haitong（萬海同），et al.Instit Cardiocerebral Vasc Dis，Zhejiang TCM Univ，Hangzhou 310053.Chin J Integr Trad&West Med 2015；35（3）：281-286.

Objective To observe the clinical effect of Yangyin Yiqi Huoxue Recipe（YYHR，the basic recipe of Yangyin Tongnao Granule）in treatment of ischemic stroke patients of deficiency of qi and yin syndrome（DQYS）and static blood obstructing collaterals syndrome（SBOCS）. Methods Totally，312 patients were assigned to the control group（86 cases）and the treatment group（226 cases）using stratified randomized allocation method.Patients in the treatment group were treated with modified YYHR，while those in the control group took Xueshuan Xinmaining.The treatment lasted 4 weeks for all.Constituent ratios of the acute stage and the recovery stage of DQYS and SBOCS and their complicated syndromes were observed in the two groups.Changes of the clinical curative effect，clinical symptoms integral，whole blood viscosity ratio，plasma viscosity ratio，hematocrit，erythrocyte sedimentation rate（ESR），total cholesterol（TC），triglyceride（TG），high density lipoprotein cholesterol （HDL-C），and low density lipoprotein cholesterol（LDL-C）were detected in the two groups before and after treatment.Results There was statistical difference in constituent ratios of the acute stage and the recovery stage of DQYS SBOCS and its complicated syndromes between the two groups（P＜0.01）.DQYS and SBOCS were basic syndrome types of the two groups.The cured and markedly effective rate was 71.24%（162/226）in the treatment group and 43.02%（37/86） in the controlgroup.The total effective rate was 91.15%（206/226）in the treatment group，higher than that of the control group（76.74%，66/86）with statistical difference（P＜0.01）.There was statistical difference in the clinical symptoms integral，whole blood viscosity ratio，plasma viscosity ratio，hematocrit，ESR，TC，TG，HDL-C，and LDL-C（P＜0.05，P＜0.01）.Conclusion Symptoms of ischemic stroke patients could be improved by modified YYHR.Indices such as the whole blood viscosity，plasma viscosity ratio，hematocrit，ESR，abnormal metabolism of blood lipids were also significantly improved. Pathological changes of blood stasis induced by qi-yin deficiency exist in ischemic stroke patients，and DQYS and SBOCS were basic syndrome types.

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2015145 Effect of Yixintai granule on mRNA and protein expression levels of AQP2in renal medulla of chronic heart failure rabbits.TANG Yun（唐云），et al.Dept Cardiol，1st Affil Hosp，Hunan TCM Univ，Changsha 410007.Chin J Integr Trad&West Med 2015；35（3）：333-337.

Objective To explore the effect of Yixintai Granule （YG）on mRNA and protein expression levels of AQP2in renal medulla of chronic heart failure（CHF）rabbits. Methods CHF rat model was established by ear marginal vein injection of adriamycin.Successfully modeled rabbits were divided into the model group，the high（8.4 g/kg），middle（4.2 g/kg），and low dose（2.1 g/kg）YG group，and the Furosemide group（2 mg/kg）.Besides，a normal control group was set up.Equal volume of physiological saline was administered to rabbits of the model group and the normal control group by gastrogavage.YG at different doses was administered to rabbits of the 3 YG groups by gastrogavage.The intervention lasted for 4 weeks，once per day.After treatment the urine volume and pathomorphological changes of renal medulla tissue were observed.mRNA and its protein expression levels of AQP2were detected.Results Compared with the normal control group，the urine volume decreased significantly，mRNA and protein expression levels of renal medulla AQP2increased significantly in the model group（all P＜0.01）.Compared with the model group，the urine volume increased significantly，and mRNA and protein expression levels of renal medulla AQP2decreased significantly in all medicated groups（all P＜0.01）.Compared with the low dose YG group，the urine volume significantly increased and the mRNA expression level of renal medulla AQP2significantly decreased in the middle and high dose YG groups（all P＜0.01）.The expression level of AQP2protein significantly decreased in the high dose YG group（P＜0.01）.Pathological changes of the renal medulla were most obviously seen in the model group.But they were alleviated to various degrees in all medicated groups.They were more obviously attenuated in the middle and high dose YG groups.Conclusion YG could improve CHF possibly through down-regulating mRNA and protein expression levels of AQP2in renal medulla，and elevating the urine volume.

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