Professor YANG Zhao-min inherited the ancient doctors'experiences about point-prescription with the principle of 'inheriting the ancients without being formalistic in the ancients,bringing new ideas without losing contact with fountainhead of TCM'. He explored new ideas based on the ancient therapy,and summed his distinctive experience up as two types:simple recipe of acupuncture and moxibustion (single point,double points,three points) and compound recipe of acupuncture and moxibustion (more than fi ve points).Those were simple-clear-essential-new in composition and form,and effective therapy in clinic.

Objective To explore the protective effects of quercetin on damage induced by oxidative stress and to clari?fy its molecular mechanism. Methods Chang liver cell cultures were randomly divided into control groups, H2O2 group and 3 doses of quercetin groups. Cell survival rate was detected with MTT. Cell apoptotic rate was measured by FACS(Fluores?cence-activated cell sorting). Intracellular reactive oxygen species (ROS) level in Chang liver cells were tested by flow cy?tometer. The DCF fluorescence intensity of DCFH-DA-stained intracellular ROS was observed by fluorescence microscope. The levels of malondialdehyde (MDA), superoxide dismutase(SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were determined in liver cells using commercial available kits. The expression of Nrf2 were detected by Western blot. Re?sults Compared with control, cell survival rate and levels of SOD, CAT and GSH-Px decreased significantly in H2O2 group (P < 0.05 ),while cell appotosis rate, content of MDA and mean fluorescence intensity(MFI) increased in H2O2 group (P <0.05). In comparison with H2O2, expression of Nrf2 protein was higher in all three quercetin treatment groups (P<0.05). Con?clusion Quercetin protected Chang liver cells from H2O2-induced oxidative stress, which may be caused by the increased ex?pressions of down stream antioxidant genes via activating the Nrf2-ARE signaling pathway.

OBJECTIVE: To determine the effect of exogenous hydrogen sulfide on experimental hepatic fibrosis in rats and its mechanism. METHODS: Wistar male rats were randomly divided into three groups: a normal control group (n=8), a model group (n=8), and a hydrogen sulfide prevention group (n=8). The rat model of hepatic fibrosis was reduced by intraperitoneal injection of carbon tetrachloride (CCl4). The prevention group, in addition to intraperitoneal injection of 40% CCl4, was intraperitoneally administered H2S once a day until 8th week. After the experiment, the liver function and liver fibrosis were assayed. Liver tissue samples were used for histopathological changes. The expression of TGF-β1 in liver tissue was detected by RT-PCR and Western blot. RESULTS: Compared with the model group, the levels of ALT, AST, HA, LN, and PC III in the sulfide group were significantly reduced (P<0.01 or P<0.05), ALB content was increased (P<0.05) in the serum, TGF-β1 expression was obviously reduced, and the degree of liver fibrosis was improved (P<0.05). CONCLUSION Exogenous hydrogen sulfide can effectively inhibit the development of hepatic fibrosis, reduce the expression of TGF-β1, and decrease the the sediment of extracellular matrix in the liver tissues.
Animals ; Carbon Tetrachloride ; Extracellular Matrix ; metabolism ; Hydrogen Sulfide ; pharmacology ; therapeutic use ; Liver ; pathology ; Liver Cirrhosis ; chemically induced ; pathology ; prevention & control ; Male ; Rats ; Rats, Wistar ; Transforming Growth Factor beta1 ; antagonists & inhibitors ; metabolism