Effect of sericin on the p38MAPK signaling pathway and NLRP3 inflammasome in the kidney of type 2 diabetic rats

The present study aimed to investigate the effects of sericin on the p38MAPK signaling pathway and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome in the kidney of rats with type 2 diabetes mellitus (T2DM). A total of 36 male Sprague-Dawley rats were randomly divided into the normal group, T2DM model group and sericin group (n=12 rats/group). A T2DM model was developed through intraperitoneal injection of streptozotocin (35 mg·kg(-1)·d(-1) for 2 consecutive days), and a high-fat and high-sugar diet. The T2DM rats in the sericin group were administered 2.4 g·kg(-1)·d(-1) sericin for 35 days, and rats in the other groups were administered an equal volume of normal saline for 35 days. Fasting blood glucose was measured using the glucose oxidase method. Kidney tissue morphology was observed by H&E staining. Immunohistochemistry, western blotting, ELISA and reverse transcription-quantitative PCR were used to detect the levels of MKK6, p38MAPK, phosphorylated (p)-p38MAPK, NF-κB, IL-1β, IL-6, NLRP3 and caspase-1 in rat kidney tissues. The results revealed that blood glucose concentration, and the expression levels of MKK6, p-p38MAPK, NF-κB, IL-1β, IL-6, NLRP3 and caspase-1 were significantly increased in the T2DM group compared with those in the normal group (P<0.05). In addition, obvious pathological changes were observed in the T2DM group. Conversely, glucose concentration, and the expression levels of MKK6, p-p38MAPK, NF-κB, IL-1β, IL-6, NLRP3 and caspase-1 were significantly reduced in the sericin group compared with those in the T2DM group (P<0.05). The pathological changes were also obviously reduced. Notably, there was no significant difference in p38MAPK expression among the three groups (P>0.05). Collectively, the present study revealed that sericin may downregulate the expression levels of MKK6, p-p38MAPK, NF-κB, IL-1β, IL-6, NLRP3 and caspase-1, and inhibit activation of renal p38MAPK signaling and NLRP3-associated inflammation, which in turn may protect against kidney damage caused by T2DM.