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微藻通过调节氧化还原状态、炎症指标和凋亡生物标志物减轻衰老大鼠的年龄相关性肝脂肪变性

Attenuation of Age-Related Hepatic Steatosis by Microalgae in Senescence Rats through the Regulation of Redox Status, Inflammatory Indices, and Apoptotic Biomarkers.

作者信息

El-Baz Farouk K, Saleh Dalia O, Abdel Jaleel Gehad A, Hussein Rehab A

机构信息

Plant Biochemistry Department, National Research Centre (NRC), 33 El Buhouth St. (Former El Tahrir St.), Dokki, Giza, P.O. 12622, Egypt.

Pharmacology Department, National Research Centre (NRC), 33 El Buhouth St. (Former El Tahrir St.), Dokki, Giza, P.O. 12622, Egypt.

出版信息

Adv Pharmacol Pharm Sci. 2020 May 1;2020:3797218. doi: 10.1155/2020/3797218. eCollection 2020.

DOI:10.1155/2020/3797218
PMID:32420546
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7211240/
Abstract

BACKGROUND

Hepatic steatosis is the most common type of chronic liver disease and is considered an established risk factor of major chronic diseases.

PURPOSE

The present study aimed to investigate the effect of , a microalga and its isolated zeaxanthin on age-related hepatic steatosis as well as their underling mechanism. . Age-related hepatic steatosis was induced in rats by intraperitoneal injection of D-galactose (200 mg/kg/day) for eight consecutive weeks. biomass (BDS; 450 mg/kg), its polar fraction (PDS; 30 mg/kg), carotenoid fraction (CDS; 30 mg/kg), and isolated zeaxanthin heneicosylate (ZH; 250 g/kg) were orally administered to D-galactose treated rats for two weeks.

METHODS

Blood samples were collected 24 hours after the last dose of treatments, animals were sacrificed, and liver tissues were isolated. Sera as well as hepatic tissue homogenates were used for further investigations. Liver tissues were also used for histopathological and immunohistochemical examinations. A computed virtual docking study for the biologically active candidates was performed to confirm the proposed mechanism of action.

RESULTS

Oral treatment of D-galactose-injected rats with BDS, PDS, CDS, or ZH ameliorated the serum hepatic function parameters as well as serum levels of adiponectin, apolipoprotein B 100, and insulin. Furthermore, decreased the hepatic lipid contents, redox status biomarkers, inflammatory cytokine, and showing antiapoptotic properties. Molecular docking of -carotene and zeaxanthin on various receptors involved in the pathophysiological cascade of steatosis highlighted the possible mechanism underlying the observed therapeutic effect.

CONCLUSION

carotenoids have beneficial effect on age-related hepatic steatosis in senescence rats through the regulation of redox status, inflammatory indices, and apoptotic biomarkers.

摘要

背景

肝脂肪变性是最常见的慢性肝病类型,被认为是主要慢性疾病的既定危险因素。

目的

本研究旨在探讨一种微藻及其分离的玉米黄质对年龄相关性肝脂肪变性的影响及其潜在机制。通过连续八周腹腔注射D-半乳糖(200mg/kg/天)诱导大鼠发生年龄相关性肝脂肪变性。将该微藻生物质(BDS;450mg/kg)、其极性组分(PDS;30mg/kg)、类胡萝卜素组分(CDS;30mg/kg)和分离的二十二碳酸玉米黄质(ZH;250μg/kg)口服给予经D-半乳糖处理的大鼠两周。

方法

在最后一剂治疗后24小时采集血样,处死动物并分离肝脏组织。血清以及肝组织匀浆用于进一步研究。肝组织也用于组织病理学和免疫组织化学检查。对生物活性候选物进行计算机虚拟对接研究以确认所提出的作用机制。

结果

用BDS、PDS、CDS或ZH口服治疗注射D-半乳糖的大鼠可改善血清肝功能参数以及脂联素、载脂蛋白B 100和胰岛素的血清水平。此外,其降低了肝脏脂质含量、氧化还原状态生物标志物、炎性细胞因子,并显示出抗凋亡特性。β-胡萝卜素和玉米黄质在参与脂肪变性病理生理级联反应的各种受体上的分子对接突出了观察到的治疗效果的潜在机制。

结论

类胡萝卜素通过调节氧化还原状态、炎性指标和凋亡生物标志物对衰老大鼠的年龄相关性肝脂肪变性具有有益作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/dba0e2351a37/APS2020-3797218.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/7902aea2c13f/APS2020-3797218.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/66cd130d8352/APS2020-3797218.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/b410ae1d373f/APS2020-3797218.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/446caa652b23/APS2020-3797218.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/0ae589368378/APS2020-3797218.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/d581ed58dc27/APS2020-3797218.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/dba0e2351a37/APS2020-3797218.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/7902aea2c13f/APS2020-3797218.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/66cd130d8352/APS2020-3797218.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/b410ae1d373f/APS2020-3797218.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/446caa652b23/APS2020-3797218.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/0ae589368378/APS2020-3797218.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/d581ed58dc27/APS2020-3797218.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35a8/7211240/dba0e2351a37/APS2020-3797218.007.jpg

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