AI Article Synopsis
- The study investigates how hydrogen sulfide (H2S) impacts kidney injury caused by ischemia/reperfusion in rats, focusing on the role of the SR-A signaling pathway in regulating stress and autophagy in kidney cells.
- Researchers used various groups of normal and SR-A knockout rats to assess kidney function and cell damage through measures like protein levels, apoptosis, and gene expression related to stress responses.
- Results indicated that H2S can help reduce kidney damage and control autophagy and stress pathways, showing that the presence of SR-A is crucial for these protective effects.
Article Abstract
Objective: This study aims to explore the effects of the exogenous hydrogen sulfide (H2S)-mediated scavenger receptor A (SR-A) signaling pathway on renal ischemia/reperfusion injury (IRI) by regulating endoplasmic reticulum (ER) stress-induced autophagy in rats.
Methods: A total of 48 normal Sprague-Dawley (SD) rats and SR-A knockout rats were selected and divided into six groups (n = 8): wild-type (WT) + sham, WT + ischemia-reperfusion (I/R), WT + I/R + NaHS, SR-A-/- + sham, SR-A-/- + I/R and SR-A-/- + I/R + NaHS. The concentrations of urinary protein, blood urea nitrogen (BUN), serum creatinine (SCR), malondialdehyde (MDA) and H2S in renal tissue were detected. qRT-PCR and Western blotting were used to detect the mRNA and protein levels of IL-6, TGF-β, SR-A, LC3I, LC3II, P62, PERK, ATF6 and IRE1 pathway-related genes. A TUNEL assay was used to detect cell apoptosis. Electron microscopy was applied to observe the structure of renal autophagosomes.
Results: Compared with the WT + sham group, in the rates of the WT + I/R group, the urine volume, urinary protein, BUN, SCR and MDA concentrations, the mRNA and protein expression of IL-6, TGF-β, LC3II/I, and ER stress pathway-related genes, the cell apoptosis index, and the number of autophagosomes were significantly increased 24 h after I/R, while P62 and SR-A protein expression and SOD and H2S concentrations were significantly decreased (all P < 0.05). The levels of renal injury, autophagy and ER stress pathway-related genes were decreased in the WT + I/R + NaHS group but were increased in the SR-A-/- + I/R group relative to the WT + I/R group. No significant differences were observed in the urine volume; the concentrations of urinary protein, BUN, SCR and MDA; the SOD activity; the mRNA and protein expression of IL-6, TGF-β, SR-A, GRP78, SR-A, GPR94, ATF4, IRE1, XBP1, ATF6, and eIF2α; the cell apoptosis index; or the number of autophagosomes in rats of the SR-A-/- + I/R and SR-A-/- + I/R + NaHS groups (all P > 0.05).
Conclusion: These results demonstrate that the exogenous H2S-mediated SR-A signaling pathway reduces renal IRI injury by up-regulating ER stress-induced autophagy in rats.
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View Article and Find Full Text PDFArticle Synopsis
- The study investigates how hydrogen sulfide (H2S) impacts kidney injury caused by ischemia/reperfusion in rats, focusing on the role of the SR-A signaling pathway in regulating stress and autophagy in kidney cells.
- Researchers used various groups of normal and SR-A knockout rats to assess kidney function and cell damage through measures like protein levels, apoptosis, and gene expression related to stress responses.
- Results indicated that H2S can help reduce kidney damage and control autophagy and stress pathways, showing that the presence of SR-A is crucial for these protective effects.
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