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姜黄素通过 NF-κB 信号通路保护大鼠的放射性肝损伤。

Curcumin protects radiation-induced liver damage in rats through the NF-κB signaling pathway.

机构信息

Department of Hepatobiliary Surgery, Affiliated Nanhua Hospital, University of South China, Hengyang, 421002, Hunan, China.

Department of Gastroenterology, Affiliated Nanhua Hospital, University of South China, Hengyang, 421002, Hunan, China.

出版信息

BMC Complement Med Ther. 2021 Jan 6;21(1):10. doi: 10.1186/s12906-020-03182-1.

DOI:10.1186/s12906-020-03182-1
PMID:33407412
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7789609/
Abstract

BACKGROUND

Curcumin has been demonstrated to exert anti-oxidant, anti-fibrotic, anti-inflammatory, and anti-cancer activities. This study was conducted to observe the effect and inner mechanism of curcumin in rats with radiation-induced liver damage (RILD).

METHODS

Thirty SD rats were classified into Control, Radiation group and Curcumin (Cur) + Radiation group (n = 10 in each group). The changes in body weight of the rats were observed on the 3rd, 7th and 14th days after the treatment with curcumin. On the 14th day post treatment, the heart blood of the rats was drawn for measurement of liver function indices including total protein (TP), alanine aminotransfetase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) as well as aspartate aminotransfetase (AST). Subsequently, the rats were euthanized and liver tissues were taken to observe liver morphological changes using hematoxylin-eosin (HE), and to analyze apoptosis condition using transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) assays. Meanwhile, the oxidative stress level in liver tissue homogenate was determined by biochemical analysis. The expression of nuclear factor kappa B (NF-κB) pathway-associated and apoptosis-associated proteins was detected using Western blot analysis, and the expression levels of inflammatory factors were measured by Enzyme-linked immunosorbent assay (ELISA).

RESULTS

The reduced body weight was observed in rats of the Radiation group compared to the Control and Cur + Radiation groups on day 14. In the Radiation group, hepatic cell edema and inflammatory cell infiltration could be visible under the light microscope, and the hepatocytes presented with vacuolar degeneration. In the Cur + Radiation group, the hepatocytes swelled under the microscope, but the pathological changes were alleviated in comparison with the Radiation group. RILD rats with curcumin treatment presented with decreased ALT, AST, ALP, LDH, and maleicdialdehyde (MDA) levels, and elevated TP, superoxide dismutase (SOD), caspase activated DNase (CAD) and glutathione (GSH) levels. Apoptosis and inflammation in rats with RILD were up-regulated, and the NF-κB pathway was activated, but they were reversed after continuously intragastric administration of curcumin for 14 days.

CONCLUSION

Our study highlights that curcumin treatment reduces the liver damage caused by radiation through the inhibition of the NF-κB pathway.

摘要

背景

姜黄素具有抗氧化、抗纤维化、抗炎和抗癌作用。本研究旨在观察姜黄素对放射性肝损伤(RILD)大鼠的作用及其内在机制。

方法

30 只 SD 大鼠分为对照组、照射组和姜黄素(Cur)+照射组(每组 10 只)。在给予姜黄素后第 3、7 和 14 天观察大鼠体重变化。治疗后第 14 天,抽取大鼠心脏血,检测肝功能指标,包括总蛋白(TP)、丙氨酸氨基转移酶(ALT)、碱性磷酸酶(ALP)、乳酸脱氢酶(LDH)和天冬氨酸氨基转移酶(AST)。随后处死大鼠,取肝组织,苏木精-伊红(HE)染色观察肝组织形态学变化,末端转移酶介导的脱氧尿苷三磷酸生物素缺口末端标记(TUNEL)检测细胞凋亡情况。同时,采用生化分析检测肝组织匀浆的氧化应激水平。采用 Western blot 检测核因子-κB(NF-κB)通路相关和凋亡相关蛋白的表达,酶联免疫吸附试验(ELISA)检测炎症因子的表达。

结果

与对照组和 Cur+照射组相比,照射组大鼠第 14 天体重减轻。在照射组,光镜下可见肝细胞水肿和炎症细胞浸润,肝细胞呈空泡变性。在 Cur+照射组,显微镜下肝细胞肿胀,但与照射组相比,病理变化减轻。姜黄素治疗的 RILD 大鼠 ALT、AST、ALP、LDH 和丙二醛(MDA)水平降低,TP、超氧化物歧化酶(SOD)、半胱天冬酶激活的 DNA 酶(CAD)和谷胱甘肽(GSH)水平升高。RILD 大鼠的细胞凋亡和炎症反应上调,NF-κB 通路被激活,但连续给予姜黄素 14 天可逆转这种情况。

结论

本研究表明,姜黄素通过抑制 NF-κB 通路减轻放射性肝损伤引起的肝损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf4e/7789609/cededb8df5f9/12906_2020_3182_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf4e/7789609/3e72403adfe5/12906_2020_3182_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf4e/7789609/154a39955147/12906_2020_3182_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf4e/7789609/e8049dd46e2f/12906_2020_3182_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf4e/7789609/cededb8df5f9/12906_2020_3182_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf4e/7789609/3e72403adfe5/12906_2020_3182_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf4e/7789609/7f2cd4cbf204/12906_2020_3182_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf4e/7789609/13cb7abdd7f5/12906_2020_3182_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf4e/7789609/154a39955147/12906_2020_3182_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf4e/7789609/e8049dd46e2f/12906_2020_3182_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf4e/7789609/cededb8df5f9/12906_2020_3182_Fig6_HTML.jpg

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