Classical prescription is extensively used by later generations for its strict compatibility, precise election of herbs and outstanding efficacy. Author studied classical prescription and got a lot from it. This article described modified Gegen Qinlian Decoction combining with Baihu Rensheng Decoction in treating typhoid relapse with excessive diarrhea and fever; Xiaoqinglong Decoction combining with Tingli Dazao Xiefei Decoction in treating multiple sarcoidosis of lung; Modified Yiyi Fuzi Baijiang Powder in treating ulcer colitis, and all the prescriptions achieved significant efficacy. So, if prescription corresponding to syndreoms, classical prescription can cure intractable and severe disease.

Objective]The article summarizes the clinical experience of CHB by professor Wang Bangcai, the famous Zhejiang TCM physician. [Methods] From following professor Wang Bangcai clinical studies, summarize the experience and thoughts of treating CHB, and for two cases. [Results] Professor Wang Bangcai thinks the cause of CHB is the incubated epidemic pathogenic factor inside the body and the invasion of exogenous pathogenic factors. Its main pathogenesis is the insufficiency of healthy qi and the excess of exogenous pathogens. Insufficiency of healthy qi is the essential factor, while the accumulation of incubated epidemic pathogen and the disorder of liver and spleen is the subordinate factor. The course of the disease is generally long, the fight between healthy qi and pathogenic factors is always prolonged, and the insufficiency of healthy qi and the excess of exogenous pathogens usually both exist. Professor Wang emphasizes that strengthening healthy qi, eliminating pathogenic factors and regulating liver and spleen to comply with their nature characters are very important in order to defeat the incubated epidemic pathogen, as well as eliminating toxin inside the body and dispersing stagnant pathogens. The following two cases both have remarkable curative results. [Conclusion]Professor Wang Bangcai has original views on CHB about the etiology,pathogenesis and syndrome differentiation,which is worthy of in-depth study and understanding.

To observe the protective e ect of oral Liuweidihuang pill combined with Shengmai capsule on heart of primary hypertension with syndrome of de ciency of both qi and yin of heart and kidney.Method:While decreasing blood pressure with Captopril,oral Liuweidihuang pill combined with Shengmai capsule was used to treat 55 cases of primary hypertension,control groups was established.BP,cardiac function,damage degree of myocardial hypertrophy and blood vessel endothelium were detected.Result:ALL the indexes above in treatment group decreased obviously,showed signi cant di erence when compared with control group.Conclusion:Oral Liuweidihuang pill combined with Shengmai capsule and Captopril has cooperative e ect of antihypertension.The combined medication can treat heart damage by reducing myocardial oxygen consumption index,reversing myocardial hypertrophy,improving left ventricular function,protecting blood vessel endothelium,and preventing arteriosclerosis.

AIM: To investigate the protective affect of salvianolic acid A on palmitic acid-induced lipotoxicity in hepatocyte and its potential molecular mechanism. METHODS: The lipotoxicity model of AML12 hepatocytes induced by PA was established. Different concentrations of Sal A (20, 40, 80, 120 μmol/L) were intervened. The hepatocyte injury was detected by the Lactate dehydrogenase (LDH) method, the intracellular triglyceride (TG) content was detected by enzyme assay and the lipid droplets were observed by Bodipy staining, cell viability was detected by MTT, Intracellular reactive oxygen species (ROS) were detected by 2'eci'- dichlorofluorescein diacetate (DCFH-DA) and fluorescence microscope. Mitochondrial membrane potential was detected by rhodamine 123 and fluorescence microscope. The expression of phosphorylation of AMP-activated protein kinase (AMPK) protein and silent information regulator 1 (SIRT1) protein were observed by Western blot. RESULTS: Model of hepatocyte lipotoxicity was established after intervented for 12 h in vitro with PA (0.5 mmol/L). Different concentrations of Sal A could significantly reduce the lipid deposition and hepatocytes injury induced by PA (P<0.05), and the protective effect was dose-dependent. Secondly, Sal A could significantly improve cell mitochondrial membrane potential (P<0.01) and abate the ROS level of hepatocytes induced by PA (P<0.01). In addition, PA could significantly inhibit AMPK and SIRT1 protein expression (P<0.05). Salvianolic acid A can significantly up-regulate SIRT1 and AMPK protein expression (P<0.05). CONCLUSION: Sal A improves PA induced lipotoxicity in hepatocyte, AMPK and SIRT1 may be a potential molecular target.

AIM: To reveal the ameliorative effect of salvianolic acid A on palmitie acid-induced lipotoxicity in H9C2 cells and to explore its potential molecular mechanisms preliminarily. METHODS: H9C2 cell were induced by palmitie acid to establish a lipotoxicity model, while salvianolic acid A was added prior to palmitie acid treatment. Lactate dehydrogenase (LDH) was employed to detect cell damage. Cell counting Kit-8 was used to detect cell viability. The changes of mitochondrial membrane potential in cardiomyocyte were observed by rhodamine 123 staining. The molecular mechanisms of the ameliorative effect of salvianolic acid A was analyzed by Western Blotting. RESULTS: Palmitie acid at a concentration of 400 μmol/L significantly caused lipotoxicity damage to H9C2 cells (P<0.05). There was no cytotoxic effect of different concentrations of salvianolic acid A (10, 20, 40, 80 μmol/L) treatment on H9C2 cells (P>0.05). Salvianolic acid A intervention significantly improved lipotoxicity-induced cell death and reduction of cell mitochondrial membrane potential (P<0.05). The activation of toll-like receptor 4 (TLR4) significantly enhanced lipotoxicity-induced cell damage (P<0.05), while inhibition of TLR4 significantly reduced palmitie acid-induced lipotoxicity (P<0.05). In addition, salvianolic acid A effectively inhibited the upregulation of TLR4 and the downstream c-Jun N-terminal kinase (JNK MAPK) of TLR4 by palmitie acid treatment (P<0.05). CONCLUSION: Salvianolic acid A effectively improves lipotoxicity-induced cardiomyocyte damage. The inhibition of p38 signaling pathway is potentially involved in its protective effect. The protective effect may be related to the inhibition of TLR4/JNK MAPK signaling pathway, providing a potential molecular target for the prevention and treatment of lipotoxic cardiomyopathy.