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目的:探讨对比剂诱导的急性肾损伤（contrast-induced acute kidney injury，CIAKI）中内源性硫化氢水平是否发生变化，补充硫化氢是否可下调Nod样受体蛋白3（Nod-like receptor protein 3，NLRP3）炎症复合体从而保护肾小管上皮细胞对抗对比剂所致的肾损伤。方法:24只体重180~220 g清洁级健康雄性Sprague-Dawley大鼠按随机数字表法分为对照组、CIAKI组（碘普罗胺2.9 g/kg）及CIAKI+NaHS组（NaHS 4 mg/kg处理3 d后予碘普罗胺2.9 g/kg）组，每组8只。对肾组织进行全转录组测序及生物信息学分析，HE、PAS染色观察肾组织病理改变，TUNEL法检测肾小管上皮细胞损伤情况，免疫荧光染色检测肾组织炎症复合体NLRP3、凋亡相关斑点样蛋白（apoptosis-associated speck-like protein containing a caspase recruitment domain，ASC）、caspase-1的表达。在人肾小管上皮细胞（HK-2细胞）中探讨硫化氢在对比剂（碘普罗胺200 mgI/ml）诱导的细胞损伤中的作用，CCK-8法测定细胞存活率。结果:与对照组相比，CIAKI组大鼠内源性硫化氢合成酶相关基因胱硫醚-β-合成酶（n CBS）、胱硫醚-γ-裂解酶（n CSE）和3-巯基丙酮酸硫转移酶（n 3-n MST）水平下降（均n P<0.05）。n CBS、n CSE和n 3-n MST基因表达水平与肾功能临床生化指标血肌酐、尿素氮和胱抑素C水平呈负相关（均n P<0.05）。与CIAKI组比较，CIAKI+NaHS组大鼠血肌酐、尿素氮及胱抑素C水平较低，肾脏病理改善，肾小管上皮细胞焦亡减少，肾组织炎症复合体NLRP3、ASC、caspase-1的水平较低（均n P<0.05）。在HK-2细胞中，对比剂+NaHS组细胞存活率高于对比剂组；应用CBS抑制剂减少内源性硫化氢水平，对比剂诱导的HK-2细胞存活率进一步降低（n P<0.05）。n 结论:内源性硫化氢系统受损是CIAKI发病的关键环节，上调硫化氢水平可改善CIAKI大鼠的肾损伤，其保护机制与调节NLRP3炎症复合体相关。“,”Objective:To investigate the level of endogenous hydrogen sulfide (Hn 2S) in contrast-induced acute kidney injury (CIAKI), as well as the potential role of Hn 2S against CIAKI by down-regulating NLRP3 inflammasome.n Methods:Twenty-four healthy male Sprague-Dawley rats, weighing 180-220 g, were randomly divided into three groups according to the random number table method: control group, CIAKI group (iopromide 2.9 g/kg) and CIAKI+NaHS group (NaHS 4 mg/kg for three days before 2.9 g/kg iopromide injection). Kidneys were collected for whole-genome sequencing and bioinformatic analysis. HE and PAS staining were used for kidney histological examination. TUNEL assays were applied to detect renal tubular epithelial injury. Expressions of NLRP3 inflammasome (NLRP3, ASC and caspase-1) were evaluated by immunofluorescence staining. The role of Hn 2S in contrast (iopromide 200 mgI/kg)-induced injury on human renal tubular epithelium (HK-2 cells) was investigated, and CCK-8 assay was used to detect cellular viability.n Results:Compared with the control group, the expression of endogenous Hn 2S synthetases-related genes [cystathionine β-synthase ( n CBS), cystathionine-γ-lyase (n CSE) and 3-mercaptopyruvate sulfurtransferase (n 3-n MST)] was lower in CIAKI group (all n P<0.05). The gene expression levels ofn CBS, n CSE and n 3-n MST were negatively correlated with renal function biomarkers serum creatinine, blood urea nitrogen and cystatin-C (all n P<0.05). Compared with the CIAKI group, CIAKI+NaHS group showed alleviated creatinine, blood urea nitrogen and cystatin-C, improved histological changes, reduced apoptosis. Moreover, the expression levels of NLRP3, ASC and caspase-1 in CIAKI+NaHS group were lower than those in CIAKI group (alln P<0.05). In HK-2 cells, compared with the contrast group, the cellular viability was higher in the contrast+NaHS group; reducing endogenous Hn 2S by CBS inhibitor could enhance contrast-induced cell viability (n P<0.05).n Conclusions:Injury of endogenous Hn 2S system is pivotal to CIAKI pathogenesis. Up-regulation of Hn 2S ameliorates renal injury of CIAKI rats, which may be related to regulation of NLRP3 inflammasome.n