ABSTRACT
Objective_To investigate the effect of ginsenoside Rg1 on the spleen structure and function of aging rats and its relative mechanism.Methods_Forty SD rats were randomly divided into normal control group, aging model group (D-galactose 120 mg/kg,qd ×42 d), Rg1 intervention group(D-galactose 120 mg/kg,qd ×42 d and Rg1 20 mg/kg, from day 15th,qd ×28 d) and Rg1 control group.After finishing injections the spleen index was meas-ured, paraffin sections were then made to observe spleen microscopic structure.Senescence-associatedβ-Galactosi-dase( SA-β-Gal) stain was used to detect aging splenocytes.The proliferative capacity of splenocytes stimulated with Concanavalin A (ConA) was measured by CCK-8.The content of IL-2,IL-6 and advanced glycosylation end products(AGEs) was detected by ELISA.The level of ROS was analyzed by flow cytometry(FCM).Malondialde-hyde(MDA), superoxide dismutase (SOD) were detected by enzymatic assay.The expression of senescence-associ-ated protein P53,P21 and RB were detected by Western blot analysis.Results_Comparing the Rg1 intervention group with the aging model group, spleen index, splenic white pulp area proportion, the proliferative capacity of splenocytes were significantly increased (P<0.05);The secretory capability of IL-2 and IL-6, the active content of SOD were obviously increased(P<0.01);The percentage of SA-β-Gal positive splenocytes, the productions of ROS and MDA were significantly decreased (P<0.01);The production of AGEs was decreased (P<0.05);The expressions of P53,P21 and Rb were also significantly down-regulated ( P<0.01) .Conclusions_Ginsenoside Rg1 relieves injure of the spleen in aging rats induced by D-galactose.It is suggested that the mechanism may be Rg1 in-hibiting oxidative stress and down-regulating P53-P21-RB signaling pathway.
ABSTRACT
Objective To investigate the anatomic feature and special clinical manifestations of variant right intrahepatic bile duct draining into left hepatic bile duct near the umbilical portion. Methods Variant right intrahepatic bile ducts joining into left hepatic bile ducts near the umbilical portions were identified through cholangiograms in 52 patients, who were included in this study. Their history, clinical process and operations were reviewed. Results There were total 38 cases of intrahepatic gallstone in this group. High incidence of intrahepatic calculi was found in variant right intrahepatic bile ducts (23/38 cases, 60.52%) and left hepatic ducts (33/38 cases, 86.84%). Most of these cases were accompanied with dilatation and stricture of bile ducts in these area. The gallstones in the variant right intrahepatic bile ducts were not detected in 8 cases (8/23) and the rate of residual gallstone was as high as 86.95%(20/23). Injury of variant right intrahepatic bile duct took place when left hepatectomy was performed in one case. Conclusion Gallstone is very likely to be formed in the variant right intrahepatic bile duct due to derangement of bile hydrokinetics and compression of blood vessel. Special attention should be paid to the diagnosis and operation of this abnormity.