Background: Intestinal ischemia-reperfusion (I/R) is a common and serious clinical condition. Lactoferrin (Lf) has displayed antioxidative and anti-inflammatory activities in protecting the intestinal mucosa. The objective of this study was to investigate whether oral administration of Lf could attenuate I/R-induced intestinal injury. Methods: The experimental design consisted of three groups of Wistar rats (24 per group): sham operation, control (I/R, saline), Lf (I/R, Lf). Intestinal I/R was produced by occlusion of the superior mesenteric artery for 45 min. Eight rats from each group were randomly sacrificed 3, 12 or 36 h after reperfusion, and blood and intestinal samples were collected. Results: Intestinal I/R resulted in gut damage evidenced by morphological alteration, reduction of γ-glutamyl transpeptidase (γ-GGT) activity and increased cell apoptosis. Daily administration of Lf (200 mg/kg) for 14 days before surgery significantly attenuated gut damage by reducing the histologic score and apoptosis index, and restoring intestinal γ-GGT activity. Lf reduced intestinal malondialdehyde and myeloperoxidase, restored glutathione and decreased serum levels of tumor necrosis factor-α, interleukin (IL)-1β and IL-6 compared with saline control in I/R rats. In addition, oral administration of Lf did not produce any significant effects in healthy rats; Lf at doses of 50 or 100 mg/kg also attenuated I/R-induced gut damage, but administration of Lf for 7 days did not exert a significant protective effect against I/R-induced gut damage. Conclusions: These results indicate that Lf may serve as a potent supplement in protecting the gut from intestinal I/R-induced injury by its antioxidative, anti-inflammatory and antiapoptotic activities.
The purpose of the study was to study the activity of the phytoestrogen genistein (GEN) acting on FSHR and LHR in rat ovaries with polycystic ovary syndrome (PCOS). Sixty rats were divided into six groups. Rats in the dose group received genistein at a concentration of either 5 (low genistein dose group, L-gen), 10 (middle genistein dose group, M-Gen) or 20 (high genistein dose group, H-Gen) mg per kg of body weight per day. Estrogen group (EG, received 0.5 mg/kg Diethylstilbestrol). Concentration of sex hormones in serum was quantified by enzyme-linked immunosorbent assay (ELISA). Expressions of follicle-stimulating hormone receptor (FSHR) and luteinizing hormone receptor (LHR) protein were determined by immunohistochemistry. Treatment with genistein resulted in a strong stimulation of the concentration of sex hormone in serum. The concentration of progesterone and FSH was significantly higher in H-Gen when compared to the PCOS model control group (MG) (P < 0.01). In contrast, the concentration of testosterone, LH and the ratio of LH/FSH decreased in GEN treatment groups compared to MG, the effect was statistically significant, tested by the ANOVA test (p<0.01). For hormone receptor activity, treatment with genistein resulted in an improvement of ovarian function with LHR protein expression being enhanced and FSHR protein expression being suppressed. Our results demonstrate that Genistein played a significant role in regulating FSH and LH receptor expression to improve perimenopausal ovarian and uterine function.
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