Liu Ying, Liao Ribin, Qiang Zhanrong, Yang Wenjun, Cao Jie
Department of Gastroenterology, The Second Affiliated Hospital of Guilin Medical University, Guilin, China.
Ann Transl Med. 2022 Jun;10(12):681. doi: 10.21037/atm-22-2126.
Hydrogen sulfide (H2S) is a newly recognized endogenously generated gasotransmitter. Endogenous H2S has been shown to be related to several gastrointestinal diseases, including irritable bowel syndrome, Crohn's disease, and ulcerative colitis. We explored the functional role of H2S in colitis and investigated the underlying mechanism.
Rats were randomly divided into control, model, and sodium hydrosulfide (NaHS) groups. Rat colitis was evaluated using the disease activity index and hematoxylin and eosin (HE) staining. The collected rat feces and intestinal charcoal transit were examined to determine intestinal motility. Enzyme-linked immunoassay kits were used to determine inflammatory factors in the rat blood. Calcium ion distribution and the protein expression of Potassium voltage gated channel subfamily D member 3 (KCND3), Maxi Potassium channel alpha (KCNMA1) and potassium inwardly rectifying channel J8 (KCNJ8) in rat smooth muscle were determined using an intracellular calcium detection kit, quantitative-reverse transcription polymerase chain reaction (qRT-PCR) and Western blot, respectively.
The results showed that H2S donor NaHS improved the intestinal mucosa of colitis rats by alleviating the tissue edema and congestion and repairing the gland structure of the intestinal mucosa. NaHS also reduced the levels of inflammatory factors containing interleukin (IL)-1β, tumor necrosis factor alpha, and IL-6 in the rat blood. Additionally, the NaHS intervention partially restored rat intestinal motility by downregulating the proteins and mRNA expression of KCND3, KCNMA1, and KCNJ8 to reconstruct the ion channels.
Our findings provide novel insights into the effect of H2S regulation on the anti-inflammatory action.
硫化氢（H₂S）是一种新发现的内源性气体递质。内源性H₂S已被证明与多种胃肠道疾病有关，包括肠易激综合征、克罗恩病和溃疡性结肠炎。我们探讨了H₂S在结肠炎中的功能作用，并研究了其潜在机制。
将大鼠随机分为对照组、模型组和硫氢化钠（NaHS）组。使用疾病活动指数和苏木精-伊红（HE）染色评估大鼠结肠炎。检查收集的大鼠粪便和肠道炭末转运情况以确定肠道蠕动。使用酶联免疫吸附测定试剂盒测定大鼠血液中的炎症因子。分别使用细胞内钙检测试剂盒、定量逆转录聚合酶链反应（qRT-PCR）和蛋白质免疫印迹法测定大鼠平滑肌中钙离子分布以及钾电压门控通道亚家族D成员3（KCND3）、大电导钙激活钾通道α亚基（KCNMA1）和内向整流钾通道J8（KCNJ8）的蛋白质表达。
结果表明，H₂S供体NaHS通过减轻组织水肿和充血以及修复肠黏膜腺体结构改善了结肠炎大鼠的肠黏膜。NaHS还降低了大鼠血液中含白细胞介素（IL）-1β、肿瘤坏死因子α和IL-6的炎症因子水平。此外，NaHS干预通过下调KCND3、KCNMA1和KCNJ8的蛋白质和mRNA表达来重建离子通道，部分恢复了大鼠肠道蠕动。
我们的研究结果为H₂S调节的抗炎作用提供了新的见解。
