Sinigrin attenuates angiotensin II‑induced kidney injury by inactivating nuclear factor‑κB and extracellular signal‑regulated kinase signaling invivo and invitro.

Abstract

The present study investigated the function of sinigrin in angiotensin II (Ang II)-induced renal damage. The results demonstrated that systolic blood pressure (SBP) and diastolic blood pressure (DBP) were increased in Ang II-challenged rats, and sinigrin treatment inhibited their increase. The levels of blood urea nitrogen (BUN) and serum creatinine (SCR) were increased by Ang II in the rats, and these were reversed by sinigrin in a dose-dependent manner. In addition, the Ang II-induced elevation of urinary protein levels was inhibited by sinigrin treatment. Glomerular basement membrane thickness and ECM degradation markers, such as collagen I, collagen IV and fibronectin, were suppressed by sinigrin in the Ang II-challenged rats. Moreover, the levels of inflammatory regulators, including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1), were reduced following sinigrin treatment of the Ang II-challenged rats and in Ang II-exposed proximal tubule epithelial cells. Furthermore, the superoxide dismutase (SOD) and catalase (CAT) levels were downregulated, whereas the malondialdehyde (MDA) levels were upregulated by Ang II; these effects were reversed by sinigrin treatment in vivo and in vitro. Mechanistically, sinigrin inhibited the Ang II-induced phosphorylation of ERK, p65 and IκBα. Thus, sinigrin attenuated Ang II-induced renal injury by inactivating ERK and NF-κB signaling. Sinigrin may thus prove to be a potential candidate for the treatment of hypertension-induced kidney damage.