李宁宁, 崔亚男, 佘晓俊, 崔博, 余善法. 噪声对大鼠肝脏形态结构和功能的影响[J]. 环境与职业医学, 2022, 39(4): 439-445. DOI: 10.11836/JEOM21389
引用本文: 李宁宁, 崔亚男, 佘晓俊, 崔博, 余善法. 噪声对大鼠肝脏形态结构和功能的影响[J]. 环境与职业医学, 2022, 39(4): 439-445. DOI: 10.11836/JEOM21389
LI Ningning, CUI Yanan, SHE Xiaojun, CUI Bo, YU Shanfa. Effect of noise on morphological structure and functions of rat liver[J]. Journal of Environmental and Occupational Medicine, 2022, 39(4): 439-445. DOI: 10.11836/JEOM21389
Citation: LI Ningning, CUI Yanan, SHE Xiaojun, CUI Bo, YU Shanfa. Effect of noise on morphological structure and functions of rat liver[J]. Journal of Environmental and Occupational Medicine, 2022, 39(4): 439-445. DOI: 10.11836/JEOM21389

噪声对大鼠肝脏形态结构和功能的影响

Effect of noise on morphological structure and functions of rat liver

  • 摘要: 背景 噪声不仅可引起听觉系统的损伤,也可致肝脏损伤,但噪声性肝损伤的生物标志和损伤机制目前尚未明确。

    目的 观察噪声对大鼠肝脏形态结构和功能的影响。

    方法 30只Wistar大鼠随机分为正常对照组、低噪声暴露组95 dB 声压级(SPL)和高噪声暴露组(105 dB SPL),噪声暴露30 d后,采血并取肝脏固定;对肝脏进行病理组织学观察,测定血清肝功能、血糖、血脂等生化指标,采用超高压液相色谱-串联四级杆飞行时间质谱(UPLC/Q-TOF-MS)联用技术检测各组大鼠的血清代谢物,鉴定代谢差异物,分析代谢通路。

    结果 噪声暴露后,与对照组相比,低、高噪声暴露组大鼠体重增长幅度降低(P<0.001,P<0.01)。病理结果显示噪声暴露的两组大鼠肝脏均有不同程度的形态结构损伤,高噪声暴露组大鼠损伤较重。与对照组相比,低噪声暴露组大鼠血清天冬氨酸转氨酶、白蛋白、糖化血清蛋白水平升高(均P<0.05),总胆汁酸水平降低(P<0.05);高噪声暴露组大鼠血清谷氨酸转氨酶、天冬氨酸转氨酶、白蛋白、甘油三酯、低密度脂蛋白、糖化血清蛋白水平升高(均P<0.05),葡萄糖水平降低(P<0.05)。血清代谢组学检测分析结果:低噪声暴露组筛选出11种差异代谢物,主要富集在硫胺素新陈代谢(thiamine metabolism)、初级胆汁酸生物合成(primary bile acid biosynthesis)、胆汁分泌(bile secretion)这3条与肝脏代谢相关的通路;高噪声暴露组筛选出4种差异代谢物,主要富集在胰岛素信号通路(insulin signaling pathway)、非酒精性脂肪肝(non-alcoholic fatty liver disease)、胆汁分泌(bile secretion)、胰岛素分泌(insulin secretion)4条不同的代谢通路,但代谢通路均涉及到胆汁酸分泌代谢。

    结论 噪声暴露可致大鼠肝组织结构发生改变和调节代谢的功能出现异常,肝组织形态损伤及代谢异常可能与胆汁酸分泌代谢通路有关。

     

    Abstract: Background Noise can cause not only auditory system injury, but also liver damage. However, the biomarkers and pathological mechanism of noise-induced liver injury are not clear yet.

    Objective To observe the effect of noise on the morphological structure and functions of rat liver.

    Methods A total of 30 Wistar rats were randomly divided into a normal control group, a low noise exposure group (95 dB sound pressure level (SPL), and a high noise exposure group (105 dB SPL). After 30 days of noise exposure, blood was collected, and livers were harvested and fixed. The pathological changes of livers were observed. The levels of biochemical indicators of liver function, blood glucose, and blood lipid were measured. Serum metabolites were detected by ultra-high-pressure liquid chromatography-tandem quadrupole time-of-flight mass spectrometry (UPLC/Q-TOF-MS). Differential metabolite markers and metabolic pathways were identified.

    Results Compared with the control group, the body weight gain decreased in the low noise group and the high noise group after noise exposure (P<0.001,P<0.05). The pathological results showed that noise caused the rat livers’ morphological and structural damage at various degrees, and damage of the high noise exposure group was more serious. Compared with the control group, the serum levels of aspartate aminotransferase, albumin, and glycosylated serum protein in the low noise exposure group were increased (P<0.05), but the total bile acid level was decreased (P<0.05). The serum levels of alanine aminotransferase, aspartate aminotransferase, albumin, triglyceride, low density lipoprotein, and glycosylated serum protein in the high noise group exposure were increased (P<0.05), but the glucose level was decreased (P<0.05). In the serum metabolomics analysis, 11 differential metabolites were screened out in the low noise exposure group, which were mainly enriched in 3 pathways (thiamine metabolism, primary bile acid biosynthesis, and bile secretion) related to liver metabolism. Four differential metabolites were screened out in the high exposure noise group, which were mainly enriched in four significantly different metabolic pathways (insulin signaling pathway, non-alcoholic fatty liver disease, bile secretion, and insulin secretion). All the metabolic pathways involved in bile acid secretion and metabolism.

    Conclusion Nosie exposure can not only damage the liver structure of rats, but also affects the metabolism functions of liver. The mechanism may be related to bile acid secretion metabolic pathway.

     

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