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In the present study, lipopolysaccharide (LPS) was injected i.v. via the tail vein (0.1 microg per mouse) to induce abortion (embryo resorption) in Kunming mice. The interleukin 10 (IL-10) contents in the uterus were assayed by ELISA. The results revealed that the IL-10 level was significantly decreased in the LPS-induced abortion group of mice compared to the controls. Use of Pentoxifylline (PXF), or a combination of Radix scutellariae and Rhizoma atractylodis reversed the LPS effects: bringing down the fetal resorption rate, and increasing the IL-10 level significantly. The study indicates that the anti-abortive effects of PXF and the combination of Radix scutellariae and Rhizoma atractylodis are closely related to up-regulation of the Th2 cytokine IL-10 at the maternal fetal interface.

This study was conducted to investigate the protective effect of lycopene on reproductive toxicity induced by in utero exposure to bisphenol A (BPA) in offspring mice. Pregnant mice in the BPA model group were given orally 500 mg/kg/day BPA from pregnant day (PD)8 to PD14. Mice of lycopene group were gavaged with 20 mg/kg/day lycopene from PD1 to PD7 and then given 500 mg/kg/day BPA from PD8 to PD14. Results showed that lycopene reduced the elevated mortality in offspring mice of the mother exposed to BPA. BPA lowered the levels of testosterone, luteinizing hormone, and follicle-stimulating hormone while lycopene treatment increased the levels significantly. BPA elevated estradiol while lycopene lowered estradiol in the offspring. BPA caused testicular damage as shown by less Leydig cells and ovarian injury as shown by less corpus granules in adult offspring, while lycopene decreased the damages. Maternal exposure to BPA increased Bax and decreased Bcl-2 in testicular and ovary tissues in the offspring mice. Lycopene decreased Bax in testis and ovary and increased Bcl-2 in ovary tissues in the offspring mice. These findings suggest lycopene has protective effects on in utero BPA exposure-induced reproductive toxicity in offspring mice.

This study evaluated the therapeutic efficacy of Schisandrin A on systemic colibacillosis of chickens. One hundred and eighty, 1-day-old Hailan Brown chickens were divided into 6 groups of 30 chickens each and assigned to the following treatments: 1) uninfected/untreated control; 2) infected Escherichia coli ; 3) infected-plus low dose of Schisandrin A therapy (50 mg/kg); 4) infected-plus medium dose of Schisandrin A therapy (100 mg/kg); 5) infected-plus high dose of Schisandrin A therapy (200 mg/kg) and 6) infected-plus antimicrobial therapy (florfenicol). Each group of chickens was placed in cages with a photoperiod of 12 h of light and 12 h of dark. Feed and water for all groups were provided ad libitum for the duration of the study. On d 14, all the chickens except the uninfected control group were intraperitoneally inoculated with a fresh culture of E. coli containing 1 × 10 8 CFU/mL. The parameters measured included: average daily weight gain ( ADG ), percent survivability, liver index, serum activity of enzymes (ALT and AST), hepatic and intestinal concentrations of TNF-α, IL-1β, IL-6, IL-8, and LPS, expression of tight junction proteins (occludin, ZO-1, and claudin-1), relative abundance of bacterial species and histopathological changes in hepatic and intestinal tissue. The results showed that the medium and high doses of Schisandrin A ameliorated the detrimental effects of colibacillosis on weight gain. Regarding organ indexes, E. coli infection induced a significant increase in liver index, all the doses of Schisandrin A produced a significant reduction of liver index in comparison to the E. coli infected control. Serum activity of ALT and AST enzymes significantly increased due to E. coli infection, with the exception of the low dose of Schisandrin A for AST enzyme activity, all the Schisandrin A treatments significantly lowered enzyme activity in comparison to the E. coli infected control. Regarding concentrations of inflammatory markers in hepatic and intestinal, E. coli infection caused a significant increase in TNF-α, IL-1β, IL-6, and IL-8, except the lowest dose of Schisandrin A for IL-1β, the rest of the doses tested were able to significantly reduced the concentrations of inflammatory markers. Concentrations of LPS in hepatic and intestinal tissues were significantly increased by E. coli infection, all doses of Schisandrin A significantly reduced the concentration of LPS in hepatic and intestinal tissue. E. coli infection significantly reduced the expression of 2 tight junction proteins (ZO-1 and Claudin-1), the higher doses of Schisandrin A were effective in significantly increasing the expression of these tight junction proteins when compared with the E. coli infected control. Taken together, these results show that...