[Effect of Kangxianling Recipe on p38MAPK/NF-KBp65 Mediated Inflammatory Factors in 5/6 Nephrectomized Mice].

Abstract

Objective To observe effects of Kangxianling Recipe ( KXLR) on p38MAPK/NF- κBp65 mediated inflammatory factors in chronic renal failure ( CRF) model mice. Methods Totally 56 C57BL/6J male mice (18 -22 g) were recruited in this experiment. Ten were randomly selected as a sham-operation group. The rest 46 mice were used for preparing CRF model by 5/6 nephrectomization. To- tally 33 successfully modeled mice were divided into the model group, the rapamycin (RAP) group, and the KXLR group according to serum creatinine (SCr) level, 11 in each group. Mice in the RAP group were administered with rapamycin (0.13 mg/100 g per day, 0. 5 mL each time) by gastrogavage. Mice in the KXLR group were administered with KXLR (2 g/100 g per day, 0. 5 mL each time) by gastrogavage. Equal volume of distilled water was administered to mice in the model group and the sham-operation group. Mice were sacrificed after 8 weeks of consecutive medication. The expression of neutrophils was ob- served using immunohistochemical assay. Expression levels of p38MAPK/NF-κB p65 protein and TNF-α/ IL-6 mRNA were detected by Western blot and Real-time PCR. Results Compared with the sham-opera- tion group, the number of positive neutrophils increased, expression levels of p38MAPK/NF-κB p65 protein and TNF-α/IL-6 mRNA were enhanced significantly in the model group (P <0. 05, P <0. 01). Com- pared with the model group, the number of neutrophils was reduced, expression levels of p38MAPK/NF- κB p65 protein and TNF-α/IL-6 mRNA were decreased significantly in the KXLR group and the RAP group (P <0. 05, P <0. 01). RAP showed better effect in decreasing p38MAPK protein expression than KXLR (P <0. 05). There was no statistical difference in the rest indices between the KXLR group and the RAP group (P >0. 05). Conclusions KXLR participated the regulation of p38MAPK/NF-κB p65 mediated in- flammation factors. It had certain improvement in renal fibrosis induced renal failure.