Findings indicate that β-carotene ameliorates CaOx crystal-induced renal injury and inflammation, at least in part through suppression of NF-κB signaling, and may offer a potential basis for the development of novel preventive and therapeutic approaches for kidney stone disease.
Preliminary data from the previously conducted in vivo CaOx mouse model study confirmed the CaOx-induced RIPK2 upregulation and strongly supports the involvement of RIPK2 in CaOx-induced renal cell damage.
G. Lahane, Arti Dhar, Audesh Bhat· Biochemical Pharmacology· 0 citations
Nephrolithiasis, particularly calcium oxalate (CaOx) stones, remains a global health burden with limited pharmacological options for recurrence prevention. In this study, we investigated the therapeutic mechanism of acacetin (ACA) using both in vitro (COM-stimulated HK-2 cells) and in vivo (glyoxylate-induced mice) mod...
Lei Jiang, Qing-Yan Xia, Zhong-Wen Hong et al.· International Immunopharmaco...· 0 citations
Exogenous nesfatin-1 mitigated oxidative, inflammatory, apoptotic, and fibrotic responses in COM-treated cells; however, these protective effects were minimal in nesfatin-1 silenced + COM cells.
G. Lahane, Arti Dhar· ACS Pharmacology & Translati...· 0 citations
It is demonstrated that the EP3 receptor mediates calcium oxalate kidney stone formation through the Ca2⁺/AKT signaling pathway and necroinflammation through the Ca2⁺/AKT signaling axis.
Jing Leng, Yang Li, Xue-Qing Tang et al.· Urolithiasis· 0 citations
Calcium oxalate (CaOx) stones are the most prevalent form of nephrolithiasis in adults. While murine models of CaOx stone disease are established, many lack translational features for therapeutic evaluation, including in vivo assessment of kidney function and molecular profiling of renal inflammation. We refined the gl...
N. Bhatt, Theresa T. Nguyen, I. Rudloff et al.· Urolithiasis· 0 citations
