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黄连解毒汤通过抑制丝裂原活化蛋白激酶信号通路发挥解热作用。

Huanglian Jiedu Decoction Exerts Antipyretic Effect by Inhibiting MAPK Signaling Pathway.

作者信息

Li Xing, Wei Shizhang, Ma Xiao, Li Haotian, Jing Manyi, Liu Honghong, Niu Shengqi, Tong Yuling, Chen Lisheng, Wei Ying, Ren Sichen, Zhao Yanling

机构信息

School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China.

Department of Pharmacy, The Fifth Medical Center of Chinese PLA General Hospital, Beijing, China.

出版信息

Evid Based Complement Alternat Med. 2021 Dec 31;2021:2209574. doi: 10.1155/2021/2209574. eCollection 2021.

DOI:10.1155/2021/2209574
PMID:35003291
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8741374/
Abstract

AIM

The aim of this study was to explore the antipyretic effect and potential mechanism of Huanglian Jiedu Decoction (HLJDD) on LPS-induced fever in rats.

MATERIALS AND METHODS

The fever rat model was established by LPS. Anal temperature of rats was measured every 1 hour after modeling. TNF-, IL-6, PGE, and cAMP in rat serum or hypothalamus tissue were detected by ELISA kit. In order to explore the potential active ingredients and mechanism of antipyretic effect of HLJDD, we predicted the underlying antipyretic mechanism by using network pharmacology and then verified its mechanism by Western Blotting.

RESULTS

The results showed that HLJDD can alleviate LPS-induced fever in rats. The expression levels of TNF-, IL-6, PGE, and cAMP in the treatment group were significantly lower than those in the model group. Western Blotting results showed that the protein expression of p-ERK, p-JNK, and p-P38 was significantly inhibited.

CONCLUSION

The findings suggest that HLJDD has a good antipyretic effect on LPS-induced fever in rats, which may be closely related to the inhibition of MAPK signaling pathway.

摘要

目的

本研究旨在探讨黄连解毒汤（HLJDD）对脂多糖（LPS）诱导的大鼠发热的解热作用及潜在机制。

材料与方法

采用LPS建立发热大鼠模型。造模后每1小时测量大鼠肛门温度。用ELISA试剂盒检测大鼠血清或下丘脑组织中的肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、前列腺素E（PGE）和环磷酸腺苷（cAMP）。为探究HLJDD解热作用的潜在活性成分及机制，我们运用网络药理学预测其潜在解热机制，然后通过蛋白质印迹法进行验证。

结果

结果显示HLJDD可减轻LPS诱导的大鼠发热。治疗组中TNF-α、IL-6、PGE和cAMP的表达水平显著低于模型组。蛋白质印迹法结果显示，磷酸化细胞外调节蛋白激酶（p-ERK）、磷酸化应激活化蛋白激酶（p-JNK）和磷酸化p38丝裂原活化蛋白激酶（p-P38）的蛋白表达受到显著抑制。

结论

研究结果表明，HLJDD对LPS诱导的大鼠发热具有良好的解热作用，这可能与抑制丝裂原活化蛋白激酶（MAPK）信号通路密切相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/1da4cdc2fdca/ECAM2021-2209574.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/9e1448016d4f/ECAM2021-2209574.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/bea9adeeafd4/ECAM2021-2209574.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/b540029085a0/ECAM2021-2209574.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/e1d5b5b75c8c/ECAM2021-2209574.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/c122a5ac12f6/ECAM2021-2209574.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/3fa93b1b0a1f/ECAM2021-2209574.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/1da4cdc2fdca/ECAM2021-2209574.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/9e1448016d4f/ECAM2021-2209574.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/bea9adeeafd4/ECAM2021-2209574.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/b540029085a0/ECAM2021-2209574.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/e1d5b5b75c8c/ECAM2021-2209574.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/c122a5ac12f6/ECAM2021-2209574.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/3fa93b1b0a1f/ECAM2021-2209574.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1011/8741374/1da4cdc2fdca/ECAM2021-2209574.007.jpg

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