Hydrogen sulfide (H₂S), along with nitric oxide (NO) and carbon monoxide (CO), proved to have renoprotective effects in various renal diseases. Therefore, this study investigated the renoprotective effect of H₂S, in a renal injury model, and its crosstalk with other gasotransmitters such as CO. Thirty-two adult rats were divided into four groups: control, gentamicin (GEN)-treated, GEN + sodium hydrosulfide (NaHS), and GEN + NaHS + zinc protoporphyrin (ZnPP) groups. GEN was used to induce renal injury, NaHS is a water-soluble H₂S, and ZnPP is a selective heme oxygenase-1 (HO-1) inhibitor used to inhibit CO synthesis in vivo. NaHS improved kidney functions in the GEN group as evidenced by significantly lower levels of renal injury markers: serum urea, creatinine, uric acid, urinary albumin excretion, and urinary albumin/creatinine. Moreover, NaHS administration to the GEN-treated group significantly lowered renal levels of NO and tumor necrosis factor-α with an increase in total antioxidant, HO-1, and interleukin-10 levels. Furthermore, NaHS administration downregulated the GEN-induced overexpression of the renal inducible nitric oxide synthase (iNOS) and upregulated the suppression of endothelial nitric oxide synthase (eNOS) with improvement in the histological examination and periodic acid Schiff (PAS) staining. However, this improvement in kidney function produced by NaHS was reduced by combination with ZnPP but still improved as compared with the GEN-treated group. The renoprotective effects of H₂S can be through its effects on renal tissue antioxidants, pro-inflammatory and anti-inflammatory cytokines, and expression of eNOS and iNOS which can be partially dependent on CO pathway via induction of HO-1 enzyme.

中文翻译：

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硫化氢肾脏保护作用：在大鼠肾脏损伤模型中，硫化氢与内源性一氧化碳之间可能存在联系。

硫化氢（H ₂ S）以及一氧化氮（NO）和一氧化碳（CO）被证明对多种肾脏疾病具有肾脏保护作用。因此，本研究调查了H ₂ S在肾脏损伤模型中的肾脏保护作用，以及其与其他气体传递剂（例如CO）的串扰。32只成年大鼠分为四组：对照组，庆大霉素（GEN）处理的组，GEN +氢硫化钠（NaHS）和GEN + NaHS +锌原卟啉（ZnPP）基团。GEN被用来诱发肾损伤，NaHS是水溶性H ₂S和ZnPP是一种选择性血红素加氧酶-1（HO-1）抑制剂，用于抑制体内CO的合成。NaHS改善了GEN组的肾脏功能，其肾损伤指标水平显着降低：血清尿素，肌酐，尿酸，尿白蛋白排泄和尿白蛋白/肌酐。此外，向GEN治疗组施用NaHS可以显着降低肾脏的NO水平和肿瘤坏死因子-α，同时增加总抗氧化剂，HO-1和IL-10的水平。此外，NaHS给药通过组织学检查和高碘酸希夫（PAS）染色的改善，下调了GEN诱导的肾脏诱导型一氧化氮合酶（iNOS）的过表达，并上调了内皮型一氧化氮合酶（eNOS）的抑制作用。然而，与GEN处理组相比，与ZnPP结合使用可减少NaHS产生的肾功能改善，但仍可改善。H的肾保护作用₂ S可以通过其对肾组织抗氧化剂，促炎和抗炎细胞因子的作用以及eNOS和iNOS的表达而发挥作用，而eNOS和iNOS的表达可能部分依赖于通过HO-1酶的诱导产生的CO途径。