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首页> 外文期刊>Ukrainian Biochemical Journal >Exogenous hydrogen sulfide for the treatment of mesenteric damage associated with fructose-induced malfunctions via inhibition of oxidative stress
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Exogenous hydrogen sulfide for the treatment of mesenteric damage associated with fructose-induced malfunctions via inhibition of oxidative stress

机译：外源硫化氢用于通过抑制氧化应激治疗与果糖诱导的故障相关的肠系膜损伤

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Remodeling of adipocytes in mesentery (AM) associated with nutritional overload from high fructose diet (HFD) is a source of several comorbidities. However, its pathogenesis is still unclear and there are no specific effective drugs for AM remodeling. Recently hydrogen sulfide (Hsub2/subS) demonstrated potent cytoprotective actions. The purpose of this study was to investigate the effects and underlying mechanisms of AM remodeling in rats fed HFD and with Hsub2/subS pre-treatment. Adult male rats on standard diet (SD, control group) or HFD that underwent acute water-immersion restraint stress (WIS) were evaluated for subcellular AM adaptive responses by electron microscopy. The effects on AM of exogenous sodium hydrosulfide (NaHS, 5.6 mg/kg/day for 9 days) and the Нsub2/subS-releasing aspirin (ASA) derivative (Hsub2/subS-ASA [ATB-340], 17.5 mg/kg/day) vs conventional ASA (10 mg/kg/day) vs vehicle were investigated. Serum glucose level, thiobarbituric acid reactive substances (TBARS), and activities of cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS) were examined biochemically using spectrophotometry. In the HFD groups, treatment with NaHS protected AM, as mesenteric microvascular endothelial and sub-endothelial structures were observed vs the vehicle-treated group that had signs of endothelial dysfunction, AM damage and dysfunctional mitochondria. The effect of Hsub2/subS-ASA was characterized by protection of AM against HFD and WIS-induced injury, with lower TBARS blood level and increased CSE and CBS activities. Carbohydrate overload for 4 weeks is sufficient to cause AM oxidative damage, mitochondrial dysfunction and endothelial changes. Hsub2/subS plays an important role in mesenteric adipocyte cellular survival against HFD-induced oxidative stress by decreasing overproduction of TBARS and mitochondrial dysfunction. The use of Hsub2/subS could lead to a novel approach for anti-obesity treatment.
机译：从高果糖饮食（HFD）相关的肠系膜（AM）中的重塑脂肪细胞是几种合并症的源泉。然而，其发病机制仍然尚不清楚，并且没有针对重塑的具体有效药物。最近硫化氢（H 2 s）显示出有效的细胞保护作用。本研究的目的是探讨喂养HFD的大鼠和H 2 预处理的大鼠中AM重塑的影响和潜在机制。通过电子显微镜评估亚细胞AM适应性反应进行急性水浸没限制应力（WIS）的标准饮食（SD，对照组）或HFD上的成年雄性大鼠。对外源氢硫化钠（NaHS，5.6mg / kg /天9天）的影响和Н<亚> 2 S释放阿司匹林（ASA）衍生物（H 2 S-ASA [ATB-340]，17.5mg / kg /天）对常规ASA（10mg / kg /天）VS车辆进行了VS载体。使用分光光度法检查生物化学上检查血清葡萄糖水平，硫氨酰氨基甲酸反应性物质（TBARS）和胱硫脲γ-裂解酶（CSE）和胱硫氨酸β-合酶（CBS）的活性。在HFD组中，观察到患有肠系膜微血管内皮和亚内皮结构的NAHS保护，VS患有内皮功能障碍的迹象，AM损伤和功能失调的线粒体。 H 2 S-ASA的作用是通过对抗HFD和WIS诱导的损伤保护，具有较低的TBARS血液水平并增加CSE和CBS活动。碳水化合物过载4周足以引起氧化损伤，线粒体功能障碍和内皮变化。 H 2 S在肠系膜adipyyte细胞存活中对HFD诱导的氧化胁迫进行了重要作用，降低了TBAR和线粒体功能障碍的过剩。 H 2 s的使用可能导致抗肥胖治疗的新方法。

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