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Scientific Reports
2024
August
;
14
(1)
Renogrit selectively protects against cisplatin-induced injury in human renal tubular cells and in Caenorhabditis elegans by harmonizing apoptosis and mitophagy
Acharya Balkrishna (1)
,
Vivek Gohel (2)
,
Nishit Pathak (2)
,
Monali Joshi (2)
,
Rani Singh (2)
,
Ankita Kumari (2)
,
Rishabh Dev (2)
,
Anurag Varshney (3)
1. Drug Discovery and Development Division, Patanjali Research Foundation, NH-58, Haridwar, Uttarakhand, 249405, India., Department of Allied and Applied Sciences, University of Patanjali, Patanjali Yog Peeth, Roorkee-Haridwar Road, Haridwar, Uttarakhand, 249405, India., Patanjali Yog Peeth (UK) Trust, 40 Lambhill Street, Kinning Park, Glasgow, G411AU, UK. 2. Drug Discovery and Development Division, Patanjali Research Foundation, NH-58, Haridwar, Uttarakhand, 249405, India. 3. Drug Discovery and Development Division, Patanjali Research Foundation, NH-58, Haridwar, Uttarakhand, 249405, India. anurag@patanjali.res.in.
Abstract
Cisplatin-induced nephrotoxicity restricts its clinical use against solid tumors. The present study elucidated the pharmacological effects of Renogrit, a plant-derived prescription medicine, using cisplatin-induced human renal proximal tubular (HK-2) cells and Caenorhabditis elegans. Quantification of phytochemicals in Renogrit was performed on HPTLC and UHPLC platforms. Renogrit was assessed in vitro in HK-2 cells post-exposure to clinically relevant concentration of cisplatin. It was observed that renoprotective properties of Renogrit against cisplatin-induced injury stem from its ability to regulate renal injury markers (KIM-1, NAG levels; NGAL mRNA expression), redox imbalance (ROS generation; GST levels), and mitochondrial dysfunction (mitochondrial membrane potential; SKN-1, HSP-60 expression). Renogrit was also found to modulate apoptosis (EGL-1 mRNA expression; protein levels of p-ERK, p-JNK, p-p38, c-PARP1), necroptosis (intracellular calcium accumulation; RIPK1, RIPK3, MLKL mRNA expression), mitophagy (lysosome population; mRNA expression of PINK1, PDR1; protein levels of p-PINK1, LC3B), and inflammation (IL-1β activity; protein levels of LXR-α). More importantly, Renogrit treatment did not hamper normal anti-proliferative effects of cisplatin as observed from cytotoxicity analysis on MCF-7, A549, SiHa, and T24 human cancer cells. Taken together, Renogrit could be a potential clinical candidate to mitigate cisplatin-induced nephrotoxicity without compromising the anti-neoplastic properties of cisplatin.
DHARA ID:
D064096
Pubmed ID:
39169052
Link To Full Paper
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