Objective To assess the influence of hepatic artery ligation on survival, hepatocyte apoptosis and regeneration of rats with obstructive jaundice. Methods Eighty adult male Wistar rats were divided into four groups: group A, suffered 70% hepatectomy+hepatic artery ligation+biliary drainage after 3 days of establishing obstructive jaundice model; group B, suffered 70% of hepatectomy+biliary drainage after 3 days of establishing obstructive jaundice model; group C, suffered 70% of hepatectomy+hepatic artery ligation after 3 days of sham operation; group D, suffered 70% of hepatectomy after 3 days of sham operation. Five rats of each group were sacrificed on 1, 2, 3, and 6 days after second operation. Liver function, hepatocyte apoptosis and liver regeneration were detected. Results Postoperative survival rates were not significantly different between group A and group B, similarly between group C and group D (allP＞0.05). There was no significantly different in liver function of group Aversus group B, and group Cversus group D (P＞0.05), but the synthesis of album on 1 d or 3 d after operation were significant difference (group Aversus group B,P＜0.05; group Cversus group D,P＜0.05). Both of the group A, group B and group C had the highest apoptotic index on 1 d after operation, whereas the group D had the lowest hepatic apoptotic index among four group after the surgery. The regeneration indexes were as follow: group D＞group C＞group B＞group A (allP＜0.05). On y 6 d after operation, the regeneration indexes of group A and group B did not increase, while those of group C and group D decreased remarkably. However, the regeneration indexes of four groups were lower than the mean level. Conclusions Hepatic artery ligation will increase hepatocyte apoptosis and weaken liver regeneration. However, for rats with obstructive jaundice, hepatic artery ligation didn't increase the risk of postoperative mortality.
ObjectiveTo investigate the effect of LOC103693069 on hypoxic apoptosis of bone marrow mesenchymal stem cells (BMSCs). Methods BMSCs from 1-week-old Sprague Dawley rat bone marrow were isolated, cultured, and passaged by the whole bone marrow adherent culture method. After identification of adipogenic, chondrogenic, and osteogenic differentiation, the 3rd generation cells were treated with hypoxia under 5%O2, 1%O2, and anaerobic conditions. After 48 hours, the cell viability, apoptosis, and apoptosis-related proteins [hypoxia inducible factor 1α (HIF-1α), Caspase-3, B cell lymphoma/leukemia 2 (Bcl-2)] expressions were detected, and normal BMSCs were used as controls. Based on the research results, the concentration group with the most obvious apoptosis was selected and used for subsequent experiments. After 48 hours of hypoxia treatment, BMSCs were taken and analyzed by gene chip and real-time fluorescence quantitative PCR (qRT-PCR) to screen the most significantly down-regulated gene and construct their high-expression, low-expression, and negative control lentiviruses; BMSCs were transfected with the different lentiviruses, respectively. After qRT-PCR detection confirmed that the transfection was successful, the BMSCs were treated with hypoxia for 48 hours to observe the cell viability and the expressions of apoptosis-related proteins. ResultsAfter cell viability, apoptosis, and apoptosis-related proteins were detected, cell apoptosis was the most significant under anaerobic conditions after 48 hours. The above indicators were significantly different from other groups (P<0.05), and this group was used for treatment conditions for subsequent experiments. Gene chip analysis showed that after 48 hours of hypoxia treatment, AC125847.1, LOC102547753, AABR07017208.2, and LOC103693069 were significantly down-regulated in BMSCs, and the expressions of LOC103693069 was the most significant down-regulation detected by qRT-PCR (P<0.05). It was selected to construct lentivirus and transfect BMSCs. Afterwards, qRT-PCR detection showed the successful transfection into the cells. After hypoxia treatment, the apoptosis rate and the expressions of apoptosis-related proteins of BMSCs overexpressed by the gene were significantly reduced (P<0.05). Conclusion LOC103693069 can relieve the hypoxic apoptosis of BMSCs.