[高压氧治疗对小鼠非酒精性脂肪肝的保护作用及机制]。

Q3 Medicine
H L Zhu, L Chen, W L Zhu, J Ding, K Jiang, H Tao, J Zhou, J Xuan, M F Yang, M Z Jiang, F Y Wang
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引用次数: 0

摘要

目的:探讨高压氧治疗小鼠非酒精性脂肪性肝病的疗效及机制。方法:将21只8周龄雄性C57BL/6J小鼠分为3组:对照组(正常饮食)、模型组(高脂高胆固醇饮食)和高压氧组(高脂高胆固醇饮食+高压氧治疗),每组7只。比较三组患者治疗后体重、血清肝酶、血脂的变化。采用苏木精-伊红染色、油红O染色、天狼星红染色、F4/80免疫组化染色观察肝组织病理变化。采用RT-qPCR和Western blot方法检测氧化应激和炎症因子的表达水平。组间比较采用单因素方差分析。结果:高压氧组小鼠肝组织病理学有明显改善。血清丙氨酸转氨酶、天冬氨酸转氨酶、胆固醇水平分别为(77.50±13.59)U/L、(156.06±23.68)U/L、(4.80±0.53)mmol/L,均显著低于模型组[(109.43±16.88)U/L、(216.62±18.79)U/L、(5.86±0.53)mmol/L, ppppppppp]。结论:高压氧治疗可通过调节小鼠氧化应激和炎症水平,减缓非酒精性脂肪肝的进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Protective effect and mechanism of hyperbaric oxygen therapy on non-alcoholic fatty liver disease in mice].

Objective: To investigate the curative effect and mechanism of hyperbaric oxygen therapy on nonalcoholic fatty liver disease in mice. Methods: Twenty-one 8-week-old male C57BL/6J mice were divided into three groups: control group (normal diet), model group (high-fat and high-cholesterol diet), and hyperbaric oxygen group (high-fat and high-cholesterol diet + hyperbaric oxygen therapy), with seven mice in each group. The changes in body weight, serum liver enzymes, and blood lipids were compared after treatment between the three groups. Hematoxylin-eosin staining, Oil Red O staining, Sirius red staining, and F4/80 immunohistochemical staining were used to observe the pathological changes in liver tissues. RT-qPCR and Western blot methods were used to detect the expression levels of oxidative stress and inflammatory factors. One-way analysis of variance was used for comparison among the groups. Results: Mice in the hyperbaric oxygen group had significantly improved liver histopathology. The serological levels of alanine aminotransferase, aspartate aminotransferase, and cholesterol were (77.50±13.59) U/L, (156.06±23.68) U/L, and (4.80±0.53) mmol/L, which were significantly lower than those in the model group [(109.43±16.88) U/L, (216.62±18.79) U/L, and (5.86±0.53) mmol/L, P<0.05], and accompanied by lower levels of lipid deposition, macrophage infiltration, and fibrosis. In addition, compared with the model group, the expression of antioxidant stress protein nuclear transcription factor erythroid 2-related factor 2 [(0.30±0.06) and (2.16±1.21), P<0.05] and heme oxygenase-1 [(0.48±0.19) and (1.01±0.18), P<0.05] in liver tissue showed an upward trend following hyperbaric oxygen treatment, which was also validated at the transcriptional level (P<0.05). Simultaneously, compared with the model group, the mRNA expressions of tumor necrosis factor-α [(2.60±0.71) and (0.66±0.15), P<0.05], interleukin-1β [(2.41±1.01) and (0.78±0.23), P<0.05], and interleukin-6 [(3.61±2.17) and (0.94±0.25), P<0.05] in the liver tissue of mice in the hyperbaric oxygen group were decreased. The tumor necrosis factor-α protein level [(7.50±4.73) and (1.05±0.58), P<0.05] and interleukin-1β [(1.65±0.35) and (1.02±0.02), P<0.05] was reduced following hyperbaric oxygen treatment compared with those in the model group. Conclusion: Hyperbaric oxygen therapy can slow down the progression of nonalcoholic fatty liver disease by regulating the levels of oxidative stress and inflammation in the mice.

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来源期刊
中华肝脏病杂志
中华肝脏病杂志 Medicine-Medicine (all)
CiteScore
1.20
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7574
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