Objective To explore the effects of galactooligosaccharide on the intestinal flora in premature rats.Methods Premature Sprague-Dawley rats were randomly divided into GOS group and control group.Premature rats in GOS group were feeding with GOS according 4 g/kg by dropper for 14 d.At 7 d and 14 d after feeding,the mental state and weight of rats were observed and recorded,the fresh feces in terminal rectum were collected to culture and count the number of colonies of bifidobacteria,lactobacillus,enterobacteria and enterococcus.Results Rats in GOS and the control group were normal growth during the administration period,mental state was not abnormal.Compared with the same time point of the control group,there was no significant difference in weight gain between the GOS group(P＞0.05).After feeding GOS for 7 d,there was no statistically significant difference between the number of colonies of bifidobacteria,lactobacillus,enterobacteri.a and enterococcus (P＞0.05).After feeding GOS for 14 d,the number of colonies of bifidobacteria and lactobacillus increased significantly(P＜0.05),while the number of enterobacteria and enterococcus decreased significantly (P ＜ 0.05).Conclusion Galactooligosaccharide could promote the proliferation of bifidobacterium and lactobacillus,inhibit the growth and reproduction of enterobacteria and enterococcus,so regulate the balance of intestinal flora.

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.