1.Bifidobacteria relieve CPFX-induced testosterone reduction in mice
Congcong XIE ; Dong ZHANG ; Shuaiyong LIU ; Helin FENG ; Li LI ; Fulu GAO ; Xiujun ZHAO
Basic & Clinical Medicine 2017;37(9):1270-1275
Objective To explore if bacillus bifidus relieve CPFX-induced testosterone reduction in mouse testes.Methods Twenty-four male mices were divided into 4 groups, then administered saline for 6 days (Sal6 group), CPFX for 6 days (A6 group), CPFX for 6 days followed by bifidobacteria treatment for the next 6 days (A6+P6 group), CPFX for 6 days and then saline for the next 6 days (A6+Sal6 group).We detected serum levels of testosterone by RIA, as well as levels of steroidogenic enzymes mRNA [cholesterol side-chain cleavage enzyme (P450scc) and steroidogenic acute regulatory protein (StAR)] and NF-E2-related factor2 (Nrf2) mRNA in testes by real-time PCR, Nrf2, heme oxygenase-1 (HO-1), and 4-hydroxy-2-nonenal (4-HNE) by Western blot and4-HNE by Immunohistochemistry.Results The A6 group had significantly lower serum testosterone levels compared with the Sal6 group (P<0.001), the A6+P6 group had significantly higher compared with the A6 (P<0.001) and A6+Sal6 groups (P<0.01).The A6 group had significantly lower StAR mRNA compared with the Sal6 group (P<0.001), the A6+P6 group had significantly higher level compared with the A6 (P<0.01) and A6+Sal6 groups (P<0.01).The A6 group had significantly lower P450scc mRNA as compared with the Sal6 group (P<0.001), the A6+P6 group had significantly higher compared with the A6 (P<0.001) and A6+Sal6 groups (P<0.05).The A6 group had significantly lower Nrf2 compared with the Sal6 group (P<0.001), the A6+P6 group had significantly higher compared with the A6(P<0.01) and A6+Sal6 groups (P<0.05).The A6 group higher 4-HNE expression compared with the Sal6 group, the A6+P6 group had significantly lower compared with the A6 (P<0.01) and A6+Sal6 groups (P<0.05).Conclusions Bifidobacteria the reduction of CPFX-induced testosterone reduction, and these effects may potentially explained by Nrf2 inflammatory signaling pathway.