文献类型：期刊文献

英文题名：Reversal of muscle atrophy by Zhimu and Huangbai herb pair via activation of IGF-1/Akt and autophagy signal in cancer cachexia

作者：Zhuang, Pengwei[1,2,3];Zhang, Jinbao[1,4];Wang, Yan[1,2];Zhang, Mixia[1,2];Song, Lili[1,2];Lu, Zhiqiang[1];Zhang, Lu[1];Zhang, Fengqi[1];Wang, Jing[1];Zhang, Yanjun[1,2];Wei, Hongjun[3];Li, Hongyan[3]

第一作者：Zhuang, Pengwei

通信作者：Zhang, YJ[1];Zhang, YJ[2]

机构：[1]Tianjin Univ Tradit Chinese Med, Chinese Mat Med Coll, 312 Anshanxi Rd, Tianjin 300193, Peoples R China;[2]Tianjin Univ Tradit Chinese Med, Tianjin State Key Lab Modern Chinese Med, 312 Anshanxi Rd, Tianjin 300193, Peoples R China;[3]Tianjin JF Pharmaland Technol Dev Co Ltd, Tianjin, Peoples R China;[4]Gansu Univ Chinese Med, Lanzhou, Gansu, Peoples R China

第一机构：Tianjin Univ Tradit Chinese Med, Chinese Mat Med Coll, 312 Anshanxi Rd, Tianjin 300193, Peoples R China

通信机构：[1]corresponding author), Tianjin Univ Tradit Chinese Med, Chinese Mat Med Coll, 312 Anshanxi Rd, Tianjin 300193, Peoples R China;[2]corresponding author), Tianjin Univ Tradit Chinese Med, Tianjin State Key Lab Modern Chinese Med, 312 Anshanxi Rd, Tianjin 300193, Peoples R China.

年份：2016

卷号：24

期号：3

起止页码：1189

外文期刊名：SUPPORTIVE CARE IN CANCER

收录：;Scopus(收录号：2-s2.0-84955743951);WOS:【SCI-EXPANDED(收录号:WOS:000369010000021)】；

基金：This work was supported by the National Natural Science Foundation of China (no. 81403213) and Program for Changjiang Scholars and Innovative Research Team in University ("PCSIRT", IRT 14R41).

语种：英文

外文关键词：Cancer cachexia; Skeletal muscle atrophy; Zhimu and Huangbai herb pair; Autophagy; IGF-1/Akt

摘要：Muscle atrophy is the prominent clinical feature of cancer-induced cachexia. Zhimu and Huangbai herb pair (ZBHP) has been used since ancient China times and have been phytochemically investigated for constituents that might cause anti-cancer, diabetes, and their complication. In this study, the effects and mechanisms of ZBHP on reversal of muscle atrophy were explored. C57BL/6 mice implanted with colon-26 adenocarcinoma were chosen to develop cancer cachexia for evaluating the effects of ZBHP on reversal of muscle atrophy. The body weight, survival time, inflammatory cytokines, and pathological changes of muscle were monitored. In addition, IGF-1/Akt and autophagy pathway members were analyzed to interpret the mechanism of drug response. The function and morphology of skeletal muscle in cachexia model were significantly disturbed, and the survival time was shortened. Consistently, inflammatory cytokines and muscle atrophy-related atrogin-1, MuRF1, and FOXO3 were significantly increased, and IGF-1/Akt and autophagy signal pathways were depressed. Treatment with ZBHP significantly alleviated tumor-free body weight reduction and cachexia-induced changes in cytokines and prolonged survival. ZBHP treatment not only inhibited the muscle atrophy-related genes but also activated the IGF-1/Akt and autophagy signal pathways to facilitate the protein synthesis. The results revealed that ZBHP treatment could inhibit the muscle atrophy induced by cancer cachexia and prolong the survival time, and ZBHP may be of value as a pharmacological alternative in treatment of cancer cachexia.