AI Article Synopsis
- Sepsis-induced acute kidney injury increases mortality rates, and the study investigates how ginsenoside Rg1 influences ferroptosis, a form of cell death, in kidney cells.
- Ginsenoside Rg1 was found to protect human renal tubular cells (HK-2) from ferroptosis induced by lipopolysaccharide (LPS) by enhancing the ferroptosis suppressor protein 1-CoQ-NAD(P)H pathway.
- The results show that Rg1 alleviates the harmful effects of sepsis on kidney cells, potentially offering a therapeutic avenue for managing acute kidney injury.
Article Abstract
Introduction: Sepsis-induced acute kidney injury is related to an increased mortality rate by modulating ferroptosis through ginsenoside Rg1. In this study, we explored the specific mechanism of it.
Methods: Human renal tubular epithelial cells (HK-2) were transfected with oe-ferroptosis suppressor protein 1 and treated with lipopolysaccharide for ferroptosis induction, and they were then treated with ginsenoside Rg1 and ferroptosis suppressor protein 1 inhibitor. Ferroptosis suppressor protein 1, CoQ, CoQH2, and intracellular NADH levels in HK-2 cells were assessed by Western blot, ELISA kit, and NAD/NADH kit. NAD/NADH ratio was also calculated, and 4-Hydroxynonal fluorescence intensity was assessed by immunofluorescence. HK-2 cell viability and death were assessed by CCK-8 and propidium iodide staining. Ferroptosis, lipid peroxidation, and reactive oxygen species accumulation were assessed by Western blot, kits, flow cytometry, and C11 BODIPY 581/591 molecular probe. Sepsis rat models were established by cecal ligation and perforation to investigate whether ginsenoside Rg1 regulated the ferroptosis suppressor protein 1-CoQ-NAD(P)H pathway .
Results: LPS treatment diminished ferroptosis suppressor protein 1, CoQ, CoQH2, and NADH contents in HK-2 cells, while facilitating NAD/NADH ratio and relative 4- Hydroxynonal fluorescence intensity. FSP1 overexpression inhibited lipopolysaccharideinduced lipid peroxidation in HK-2 cells the ferroptosis suppressor protein 1-CoQ- NAD(P)H pathway. The ferroptosis suppressor protein 1-CoQ-NAD(P)H pathway suppressed lipopolysaccharide-induced ferroptosis in HK-2 cells. Ginsenoside Rg1 alleviated ferroptosis in HK-2 cells by regulating the ferroptosis suppressor protein 1-CoQ- NAD(P)H pathway. Moreover, ginsenoside Rg1 regulated the ferroptosis suppressor protein 1-CoQ-NAD(P)H pathway .
Conclusion: Ginsenoside Rg1 alleviated sepsis-induced acute kidney injury by blocking renal tubular epithelial cell ferroptosis the ferroptosis suppressor protein 1-CoQ- NAD(P)H pathway.
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| http://dx.doi.org/10.2174/0929867330666230607125054 | DOI Listing |
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