Objective: To investigate the effect of the ethanolic extract of Rosa laevigata Michx. fruit on rats with mesangial proliferative glomerulonephritis based on the NLRP3 inflammasome pathway. Methods: Thirty Wistar rats were divided into three groups, a blank control group, a diabetic nephropathy (DN) model group, and an ethanolic extract intervention group, according to the random number table method, with 10 rats in each group. One day before the experiment, basic feeding was initiated for all the rats; the changes in activity and weight of each group of rats were observed and recorded after 7 d, and a rat model of renal function injury was established after 1 d. Results: Compared with the control group, the model group had significantly higher kidney/body ratio, 24 h urine protein, serum creatinine (SCr), blood urea nitrogen (BUN), glomerular mesangial cell (GMC) count, and extracellular matrix (ECM) positive area ratio (P < 0.05); the same indicators were  significantly lower in the intervention group than in the model group (P < 0.05). The NLRP3 inflammasome pathway in renal intrinsic cells was activated in the intervention group. The overactivation of NLRP3 inflammasome is known to promote interleukin (IL)-1? release, which was inhibited in the intervention group. Conclusion: The ethanolic extract of Rosa laevigata Michx. fruit has a protective effect on renal intrinsic cells and may be related to NLRP3 inflammasome pathway, suggesting that the fruit of Rosa laevigata Michx. has a potential role in protecting renal intrinsic cells from inflammatory damage. NLRP3 inflammasomes are involved in the development of various chronic inflammatory diseases, such as acute and chronic glomerulonephritis and renal fibrosis.

Objective: To investigate the effect nano-sustained CO-releasing molecules on cyclosporin-A (CsA)-induced nephrotoxicity by inhibiting the NLRP3 inflammasome-mediated TGF-β/Smad signaling pathway. Methods: 3×105 cell/mL human renal tubular epithelial cells (HK-2) and mouse primary cultured renal tubular epithelial cells (RTECs) were cultured under an inverted microscope and incubated with 10% DMEM and 0.25% β2M in NaCl solution for 3 h. HK-2 and RTECs were divided into 5 complex numbers. MTT assay was used to detect the relative proliferation level of one of the HK-2 cells and calculate the multiplication ratio. Results: The nano-sustained CO-releasing molecules CS-CO had a strong protective effect on the kidney. HK-2 and RTECs cells were treated with siRNA, inhibitors, and NLRP3 knockout mice, and the changes in cell activity and expression of intracellular inflammatory factors were studied. The expression of TGF-β1/Smad signaling pathway related proteins in HK-2 and RTECs was detected by ELISA, western blot, immunofluorescence, and other techniques. Conclusion: SMA/CORM2 alleviates CsA-induced renal fibrosis by inhibiting NLRP3 inflammasome-mediated TGF-β/Smad signaling pathway.

Objective: To investigate the expression of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and transforming growth factor beta 1 (TGF beta 1) in the kidney tissue of rats with pyelonephritis and their relationship with pyelonephritis by establishing a rat model of acute pyelonephritis. Methods: 80 male Wistar rats were randomly divided into a control group and an experimental group, with 40 rats each. The rats of the control group were injected with and saline and those of the experimental group were injected with 10 ?g/mL Escherichia coli (E. coli) and saline (1:100); the solutions for both groups were administered every 3 days for 7 days. The expressions of MMP-2, MMP-9 and TGF beta 1 in the kidney tissues of rats in each group were observed. Results: The expression of MMP-9 and TGF beta 1in the kidney tissue of rat acute pyelonephritis model rats was significantly higher than those of the control group (P < 0.01); the MMP-9 mRNA content in the kidney tissue of the experimental group was significantly higher than that of the control group (P < 0.05); the TGF beta 1 mRNA content in the renal tissue of the experimental group increased significantly compared to the  (P < 0.05); MMP-2, MMP-9 and TGF beta 1 began to express in the early stage of pyelonephritis until the complete formation of renal pelvic edema. The difference between groups was statistically significant (P < 0.01). Conclusion: MMP-9 and TGF beta 1 are important factors regulating renal tubular epithelial cell injury and inflammatory response.