Objective:To investigate the protective effects of Ruanmai Capsules on cerebral ischemia-reperfuse injury in rats.Methods:A cerebral ischemia-reperfuse model in rats was established by ligaturing bilateral arterial carotis communis and vagus nerve. NO, 6-keto-PGF 1a and TXB 2 in serum were examined. Results: Ruanmai Capsule (0.81g/kg and 2.43g/kg,po) increased the levels of NO, 6-keto-PGF 1a. It also had the tendency to decrease TXB 2 in serum. Conclusions: Ruanmai capsules can alleviate brain injury caused by cerebral ischemia reperfusion. The effect is achieved perhaps by inhibiting platelet aggregation and increasing NO.

Background Parathion and methyl parathion are typical organophosphorus insecticides and para−nitrophenol (PNP) is their main specific metabolite. Previous studies have shown that parathion and methyl parathion may play a role as endocrine disrupting chemicals, but the evidence is limited. Objective Our aim is to evaluate association between urinary PNP concentration and thyroid function among healthy adults and whether this association has gender differences. Methods The study was based on the 2007—2008 US National Health and Nutrition ExaminationSurvey (NHANES). A total of 1071 subjects aging from 20 to 64 years with data on both urinary PNP and serum thyroid function indicators were finally enrolled. Thyroid function was evaluated by measuring serum thyroid stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4), total triiodothyronine (TT3), total thyroxine (TT4), thyroglobulin (TG), and thyroglobulin antibody (TG-Ab). A generalized linear model was used to analyze the relationship between urinary PNP and serum thyroid function indicators and the dose-response relationship. Gender differences were also explored. Results In the total population, the positive rate of PNP was 92.5%, and the median urinary PNP concentration adjusted for urinary creatinine was 0.62 μg·g⁻¹. The median creatinine-adjusted urinary PNP concentrations in the male and female populations were 0.60 and 0.66 µg·g⁻¹ respectively. The median activities or concentrations of serum thyroid function indicators TSH, FT3, FT4, TT3, and TT4 in the total population were 1500.00 μIU·L⁻¹, 3200.00 pg·L⁻¹, 8.00 ng·L⁻¹, 1140.00 ng·L⁻¹, and 76.00 μg·L⁻¹ respectively. In the total population, a logarithmic unit increase of urinary PNP was associated with 1050.00 pg·L⁻¹ decrease in serum FT3 levels (b=−0.02, 95%CI: −0.02-−0.01), 10.50 ng·L⁻¹ decrease in FT4 levels (b=−0.02, 95%CI: −0.03-−0.01), and 10.50 ng·L⁻¹ decrease in TT3 levels (b=−0.02, 95%CI: −0.03-−0.01), all in a dose-response manner (all P_trend<0.05). After sex stratification, for every logarithmic unit increase of urinary PNP, the serum TG-Ab level was increased by 1100.00 IU·L⁻¹ (b=0.04, 95%CI: 0.00-0.08) and the serum FT3 level was reduced by 1020.00 pg·L⁻¹ (b=−0.01, 95%CI: −0.02-0.00) among males, and both showed dose-response relationships (both P_trend<0.05); every logarithmic unit increase of urinary PNP was associated with 1050.00 pg·L⁻¹ decrease in FT3 levels (b=−0.02, 95%CI: −0.03-−0.01), 10.50 ng·L⁻¹decrease in FT4 levels (b=−0.02, 95%CI: −0.03-0.00), 10.70 ng·L⁻¹ decrease in TT3 levels (b=−0.03, 95%CI: −0.05-−0.01), and 10.50 μg·L⁻¹ decrease in TT4 levels (b=−0.02, 95%CI: −0.04-0.00) among females, and there were dose-response relationships of urinary PNP concentration with serum FT3 and TT3 levels (both P_trend<0.001). Conclusion Changes in the concentration of PNP in urine are associated with changes in serum FT4, FT3, and TT3 levels and the results also show gender differences.