ABSTRACT
Objective: To investigate the protective effect of panaxdol saponins (PDS) on the acute liver damage (ALD) of the rats induced by carbon tetrachloride (CC14), and to clarify its mechanism. Methods: Fifty rats were randomly divded into control group (the rats were given normal saline), model group (the ALD models were established and given normal saline) and low, mddle, and hgh doses (10, 20, and 40 mg middot; kg-1) of PDS groups, and there were 10 rats in each group. The general state of the rats in various groups was observed. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), and total protein (TP) of the rats in various groups were detected; ELISA method was used to detecet the levels of interleukin-6 (IL-6), interleukin-12 (IL-12) and tumor necrosis factor-α (TNF-α) in liver tissue homogenate of the rats in various groups; Western blotting method was used to detecet the expresson levels of protein kinase B (AKT) and p-protein kinase B (p-AKT) in liver tssue of the rats in various groups. Results: Compared with control group, the levels of ALT, AST and TBIL of the rats in model group were increased (P<0. 01), and the level of TP was decreased (P<0. 01); the levels of IL-12, IL-6 and TNF-α were increased (P<0. 01). Compared with model group, the hepatic function of the rats in different doses of PDS groups were obvously improved, the levels of ALT, AST and TBIL in liver tissue of the rats in different doses of PDS groups were decreased (P<0. 01), the levels of TP were increased (P<0. 01); the levels of IL-12, IL-6 and TNF-α in liver tissue of the rats were decreased (P<0. 01); the expresson levels of AKT protein in liver tissue of the rats were decreased (P<0. 01) and the expresson level of p-AKT was increased (P<0. 01). Conclusion: PDS has the protective effect on ALD, and its mechanism may be related to reducing the expressons of inflammatory factors and affecting the p-AKT-AKT gnal pathway.
ABSTRACT
Aim To investigate the inhibitory effects of urocortin2 (UCN2) on ventral tegmental area (VTA) nervous activity of morphine addiction rats and the mechanism. Methods Morphine addiction rats and the microiontophoresis method were used to observe the effects of UCN2 on VTA neuron′s spontaneous dis-charge changing rule, as well as the inhibitory effects of UCN2 on DA neuron′s cluster spontaneous dis-charge, to identify UCN2 and DA on the same VTA neuron. Morever, the inhibitor of corticotropin-regula-ting factor′s receptor ( CRF-2 R ) and the blocker of protein kinase A ( PKA ) , AST-2 B and H89 , were used to investigate the effects of UCN2 on VTA neuron′s of morphine addiction rats. Results UCN2 could inhibit the firing rate 82% (31/38) of the tested VTA neuron ( P<0. 01 ) , the discharge frequency changed from (20. 89 ± 2. 86) Hz to (13. 66 ± 3. 93) Hz (P<0. 01). Further, the inhibitor of PKA, AST-2B and H89 could ablolish the inhibitory effects of UCN2 . Morever, the excitatory firing of VTA neurons was at-tenuated by addition of UCN2 , while AST application could inhibit the UCN2′s inhibitory effects. Conclu-sion UCN2 could regulate the effects of VTA via PKA pathway and may thereby contribute to the improvement of drug addiction.