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Renal injury is reported to have a high mortality rate. Additionally, there are several limitations to current conventional treatments that are used to manage it. This study evaluated the protective effect of hesperidin against ischemia/reperfusion (I/R)-induced kidney injury in rats. Renal injury was induced by generating I/R in kidney tissues. Rats were then treated with hesperidin at a dose of 10 or 20 mg/kg intravenously 1 day after surgery for a period of 14 days. The effect of hesperidin on renal function, serum mediators of inflammation, and levels of oxidative stress in renal tissues were observed in rat kidney tissues after I/R-induced kidney injury. Moreover, protein expression and mRNA expression in kidney tissues were determined using Western blotting and RT-PCR. Hematoxylin and eosin (H&E) staining was done for histopathological observation of kidney tissues. The data suggest that the levels of blood urea nitrogen (BUN) and creatinine in the serum of hesperidin-treated rats were lower than in the I/R group. Treatment with hesperidin also ameliorated the altered level of inflammatory mediators and oxidative stress in I/R-induced renal-injured rats. The expression of p-IκBα, caspase-3, NF-κB p65, Toll-like receptor 4 (TLR-4) protein, TLR-4 mRNA, and inducible nitric oxide synthase (iNOS) was significantly reduced in the renal tissues of hesperidin-treated rats. Histopathological findings also revealed that treatment with hesperidin attenuated the renal injury in I/R kidney-injured rats. In conclusion, our results suggest that hesperidin protects against renal injury induced by I/R by involving TLR-4/NF-κB/iNOS signaling.

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The aim of the present study was to investigate whether co-administration of nerve growth factor (NGF) and butyrate regulates vanilloid receptor 1 (VR1) and substance P (SP) levels in cultures of rat dorsal root ganglion (DRG) neurons. DRG was dissected out from embryonic 15-day-old Wistar rat and cultured as dissociated cells for 2 days then exposed to NGF (10 ng/ml), butyrate (1 mmol/L), NGF (10 ng/ml) plus butyrate (1 mmol/L) for another 4 days. The neurons cultured continuously in media served as normal control. After that, the cultures were processed for detecting expression of mRNA for VR1 and SP in DRG neurons by RT-PCR, and expression of VR1 protein by Western blot. SP basal release levels were measured by radioimmunoassay (RIA). Capsaicin-evoked SP release was measured by RIA after stimulation with capsaicin (100 nmol/L) for 10 minutes. The neurons exposed to vehicle solution served as vehicle control. Either NGF (10 ng/ml) or butyrate (1 mmol/L) promoted expression of SP mRNA, VR1 mRNA, and VR1 protein in DRG neurons and capsaicin-evoked SP release from DRG neurons. Co-administration of NGF and butyrate showed a synergistic effect on expression of VR1 mRNA, and VR1 protein in DRG neurons and capsaicin-evoked SP release from DRG neurons and a ceiling effect on SP mRNA expression. The elevation of SP mRNA, VR1 mRNA, and VR1 protein promoted by NGF and/or butyrate may be associated with increases of SP release evoked by capsaicin. The mechanisms of the effects of co-administration of NGF and butyrate should be clarified by further study.

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