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布廷总生物碱通过抑制大鼠中RANKL诱导的NF-κB和c-Fos/NFATc1信号通路减轻Walker 256诱导的骨痛和破骨细胞生成。

Bunting Total Alkaloids Attenuate Walker 256-Induced Bone Pain and Osteoclastogenesis by Suppressing RANKL-Induced NF-κB and c-Fos/NFATc1 Pathways in Rats.

作者信息

Ju Linjie, Hu Peipei, Chen Ping, Wu Jiejie, Li Zhuoqun, Qiu Zhixia, Cheng Jun, Huang Fang

机构信息

Department of Chinese Pharmacology and Traditional Chinese Medicine, China Pharmaceutical University, Nanjing, China.

Nanjing Zhongshan Pharmaceutical Co, Ltd., Nanjing Economic and Technological Development Zone, Nanjing, China.

出版信息

Front Pharmacol. 2021 Jan 26;11:609119. doi: 10.3389/fphar.2020.609119. eCollection 2020.

DOI:10.3389/fphar.2020.609119
PMID:33574755
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7870471/
Abstract

Metastatic bone pain is characterized by insufferable bone pain and abnormal bone structure. A major goal of bone cancer treatment is to ameliorate osteolytic lesion induced by tumor cells. Bunting total alkaloids (CSBTA), the alkaloid compounds extracted from the root of Bunting, have been shown to possess anticancer and analgesic properties In this study, we aimed to verify whether CSBTA could relieve cancer induced bone pain and inhibit osteoclastogenesis. The results showed that CSBTA ameliorated Walker 256 induced bone pain and osteoporosis in rats. Histopathological changes also supported that CSBTA inhibited Walker 256 cell-mediated osteolysis. Further analysis confirmed that CSBTA reduced the expression of RANKL and downregulate the level of RANKL/OPG ratio in breast cancer cells. Moreover, CSBTA could inhibit osteoclastogenesis by suppressing RANKL-induced NF-κB and c-Fos/NFATc1 pathways. Collectively, this study demonstrated that CSBTA could attenuate cancer induced bone pain via a novel mechanism. Therefore, CSBTA might be a promising candidate drug for metastatic bone pain patients.

摘要

转移性骨痛的特征是难以忍受的骨痛和异常的骨骼结构。骨癌治疗的一个主要目标是改善肿瘤细胞诱导的溶骨性病变。布氏总生物碱（CSBTA）是从布氏根中提取的生物碱化合物，已被证明具有抗癌和镇痛特性。在本研究中，我们旨在验证CSBTA是否能缓解癌症引起的骨痛并抑制破骨细胞生成。结果表明，CSBTA改善了Walker 256诱导的大鼠骨痛和骨质疏松症。组织病理学变化也支持CSBTA抑制Walker 256细胞介导的骨溶解。进一步分析证实，CSBTA降低了乳腺癌细胞中RANKL的表达并下调了RANKL/OPG比值水平。此外，CSBTA可通过抑制RANKL诱导的NF-κB和c-Fos/NFATc1途径来抑制破骨细胞生成。总体而言，本研究表明CSBTA可通过一种新机制减轻癌症引起的骨痛。因此，CSBTA可能是转移性骨痛患者的一种有前途的候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d363/7870471/25058ce4b5da/fphar-11-609119-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d363/7870471/8001d712f365/fphar-11-609119-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d363/7870471/81b43e447c5e/fphar-11-609119-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d363/7870471/25058ce4b5da/fphar-11-609119-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d363/7870471/466d6c98792b/fphar-11-609119-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d363/7870471/325ff0c42db9/fphar-11-609119-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d363/7870471/0366c12f8f34/fphar-11-609119-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d363/7870471/8001d712f365/fphar-11-609119-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d363/7870471/0bb958b628af/fphar-11-609119-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d363/7870471/25058ce4b5da/fphar-11-609119-g008.jpg

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