Objective To explore the mechanism of Dahuanglinxian Capsule for intervening gallstone formation by regulating the expression levels of ABCB11 and ABCC2 mRNA and protein.Methods Forty male C57BL/6 mice were divided into the normal group(group N),model group (group M),ursodeoxycholic acid group (group U) and Dahuanglinxian Capsule treatment group (group D),10 cases in each group.The group N was fed with normal diet,while the group M,U and D were fed with lithogenic fodder for 8 weeks.Meanwhile the group U and D were given the medication intervention,once daily,for continuous 8 weeks of gavage.After successful modeling,mRNA and protein expression levels of ABCB11 and ABCC2 were detected by RT-PCR and immunohistochemistry.Results Compared with the other three groups,the expressions of ABCB11 and ABCC2 mRNA gene and protein in M group were significantly reduced(P＜0.01);while,there was no statistical difference in the expressions of ABCB11 and ABCC2 mRNA and protein between the group D and N(P＞0.05).Conclusion Dahuanglinxian Capsule can prevent the gallstone formation by regulating the expression of ABCB11 and ABCC2 mRNA and protein.

Metabolic reprogramming is a hallmark of cancer, including lung cancer. However, the exact underlying mechanism and therapeutic potential are largely unknown. Here we report that protein arginine methyltransferase 6 (PRMT6) is highly expressed in lung cancer and is required for cell metabolism, tumorigenicity, and cisplatin response of lung cancer. PRMT6 regulated the oxidative pentose phosphate pathway (PPP) flux and glycolysis pathway in human lung cancer by increasing the activity of 6-phospho-gluconate dehydrogenase (6PGD) and α-enolase (ENO1). Furthermore, PRMT6 methylated R324 of 6PGD to enhancing its activity; while methylation at R9 and R372 of ENO1 promotes formation of active ENO1 dimers and 2-phosphoglycerate (2-PG) binding to ENO1, respectively. Lastly, targeting PRMT6 blocked the oxidative PPP flux, glycolysis pathway, and tumor growth, as well as enhanced the anti-tumor effects of cisplatin in lung cancer. Together, this study demonstrates that PRMT6 acts as a post-translational modification (PTM) regulator of glucose metabolism, which leads to the pathogenesis of lung cancer. It was proven that the PRMT6-6PGD/ENO1 regulatory axis is an important determinant of carcinogenesis and may become a promising cancer therapeutic strategy.