TY  - JOUR
TI  - Panax notoginseng saponins ameliorate renal interstitial fibrosis in a rat model of chronic kidney disease via the TLR4/NF-κB signaling pathway
AU  - Zhao, Xiaodong
AU  - Wang, Zhenzhen
AU  - Zhang, Hongmei
AU  - Ren, Jianmin
JO  - Pakistan Journal of Pharmaceutical Sciences
JA  - Pak. J. Pharm. Sci.
VL  - 39
IS  - 5
SP  - 1520
EP  - 1528
PY  - 2026
DA  - 2026/05
KW  - PNS
KW  - Renal interstitial fibrosis
KW  - TLR4/NF-κB pathway
KW  - TGF-β1
DO  - 10.36721/PJPS.2026.39.5.REG.15768.1
AB  - Background: Renal interstitial fibrosis (RIF) is a central pathological process in the progression of chronic kidney disease (CKD), and effective therapeutic drugs remain limited. Panax notoginseng saponins (PNS) demonstrate potential anti-inflammatory and anti-fibrotic properties, though their mechanisms in RIF are not fully understood. Objectives: To investigate the therapeutic effects of PNS on renal interstitial fibrosis in a rat CKD model and determine whether these effects involve regulation of the TLR4/NF-κB signaling pathway. Methods: A rat CKD model was established with groups including healthy control, model, PNS-treated, TAK-242-treated, LPS-treated and combination groups (PNS+TAK-242 and PNS+LPS). Renal pathology and fibrosis were assessed using HE and Masson staining, while fibrosis markers and TLR4/NF-κB pathway molecules were evaluated using RT-qPCR and Western blot. Results: PNS treatment significantly alleviated renal tissue injury and reduced fibrotic areas compared with the model group. It also downregulated gene and protein expression of fibrosis markers, TLR4 and Rel (NF-κB p65). The TLR4 inhibitor TAK-242 produced anti-fibrotic effects similar to PNS, and the combination of PNS with TAK-242 produced the strongest therapeutic effect. Conclusion: PNS markedly alleviates renal interstitial fibrosis in CKD model rats, likely through inhibition of the TLR4/NF-κB signaling pathway and subsequent downregulation of downstream pro-fibrotic factors.
ER  -