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使用富氢水对抗庆大霉素诱导的肾毒性中的氧化应激和炎症。

Combating oxidative stress and inflammation in gentamicin-induced nephrotoxicity using hydrogen-rich water.

作者信息

Cumaoglu Mustafa Oguz, Makav Mustafa, Dag Serpil, Uysal Ayfer Yildiz, Baser Lale, LeBaron Tyler W, Alwazeer Duried

机构信息

Niğde Ömer Halisdemir University, Faculty of Medicine, Department of Emergency Medicine, Niğde, Türkiye.

Kafkas University, Faculty of Veterinary Medicine, Department of Physiology, Kars, Türkiye.

出版信息

Tissue Cell. 2024 Dec;91:102604. doi: 10.1016/j.tice.2024.102604. Epub 2024 Nov 5.

DOI:10.1016/j.tice.2024.102604
PMID:39531856
Abstract

Gentamicin-induced nephrotoxicity primarily results from renal inflammatory cascades and increased oxidative stress. This study aims to examine the effects of hydrogen-rich water (HRW) on gentamicin-induced renal damage in rats. Thirty-two rats were equally divided into four groups, including control (no treatment), hydrogen, gentamicin, and gentamicin+hydrogen. At the end of one week, all animals were euthanized following ethical rules, and blood and tissue samples were analyzed for examining Malondialdehyde (MDA), glutathione (GSH), Tumor Necrosis Factor-Alfa (TNF-α), Tumor Necrosis Factor-Beta (TNF-β), Interleukin 6 (IL-6), endoglin, endocan, urea, creatinine, Na, and K parameters. Levels of 8-Hydroxyguanosine (8-OHdG), MDA, and Bax were immunohistochemically analyzed. Data showed that while MDA (control P<0.0001, HP<0.0001, ‎Genta+HP<0.0007), TNF-α (control P<0.0002, HP<0.0040, ‎Genta+HP<0.0381), IL-6 (control P<0.0044, HP<0.0070, ‎Genta+HP<0.0109), endocan (control P<0.0460, HP<0.0286, ‎Genta+HP<0.0452), and endoglin (control P<0.0131, HP<0.0164, ‎Genta+HP<0.0397), urea (control P<0.0024, HP<0.0001, ‎Genta+HP<0.0180), and creatinine parameters (control P<0.0017, HP<0.0178, ‎Genta+HP<0.0011) increased in the gentamicin group compared to the other groups, a decrease in these parameters was observed in the gentamicin+hydrogen group compared to the gentamicin group. The Genta group had greater levels of TNF-β than the control (P<0.0042) and H2 groups (P<0.0268). GSH content was higher in the hydrogen group compared to the gentamicin group. Immunohistochemically, 8-OHdG, MDA, and Bax expressions increased in the gentamicin group compared to the control group, whereas they decreased in the gentamicin+hydrogen group compared to the gentamicin group. Hydrogen may be an alternative treatment for oxidative stress-induced nephrotoxicity.

摘要

庆大霉素诱导的肾毒性主要源于肾脏炎症级联反应和氧化应激增加。本研究旨在探讨富氢水(HRW)对庆大霉素诱导的大鼠肾损伤的影响。32只大鼠平均分为四组,包括对照组(未治疗)、氢组、庆大霉素组和庆大霉素+氢组。一周结束时,按照伦理规则对所有动物实施安乐死,并对血液和组织样本进行分析,以检测丙二醛(MDA)、谷胱甘肽(GSH)、肿瘤坏死因子-α(TNF-α)、肿瘤坏死因子-β(TNF-β)、白细胞介素6(IL-6)、内皮糖蛋白、内皮抑素、尿素、肌酐、钠和钾参数。采用免疫组织化学方法分析8-羟基鸟苷(8-OHdG)、MDA和Bax的水平。数据显示,与其他组相比,庆大霉素组的MDA(对照组P<0.0001,氢组P<0.0001,庆大霉素+氢组P<0.0007)、TNF-α(对照组P<0.0002,氢组P<0.0040,庆大霉素+氢组P<0.0381)、IL-6(对照组P<0.0044,氢组P<0.0070,庆大霉素+氢组P<0.0109)、内皮抑素(对照组P<0.0460,氢组P<0.0286,庆大霉素+氢组P<0.0452)和内皮糖蛋白(对照组P<0.0131,氢组P<0.0164,庆大霉素+氢组P<0.0397)、尿素(对照组P<0.0024,氢组P<0.0001,庆大霉素+氢组P<0.0180)以及肌酐参数(对照组P<0.0017,氢组P<0.0178,庆大霉素+氢组P<0.0011)均升高;与庆大霉素组相比,庆大霉素+氢组这些参数有所降低。庆大霉素组的TNF-β水平高于对照组(P<0.0042)和氢组(P<0.0268)。氢组的GSH含量高于庆大霉素组。免疫组织化学结果显示,与对照组相比,庆大霉素组的8-OHdG、MDA和Bax表达增加;而与庆大霉素组相比,庆大霉素+氢组的这些表达降低。氢可能是氧化应激诱导的肾毒性的一种替代治疗方法。

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