穿心莲内酯和吡非尼酮联合给药对TGF-β1诱导的肝星状细胞活化的影响及作用机制

doi:10.3969/j.issn.1671-7171.2022.02.003

Abstract
Figure/Table
References
Related Citation (15)

Download: PDF (1591 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract 【Objective】To investigate the effect of andrographolide (AG) combined with pirfenidone (PFD) on hepatic stellate cell activation induced by transforming growth factor-β1(TGF-β1) and its mechanism . 【Methods】 Hepatic stellate cells (LX-2) were used as the research object. After routine in vitro culture, they were divided into control group, TGF-β1 Group , AG group, PFD group and AG + PFD group. MTT assay was used to determine the cell viability of five groups, RT-PCR was used to detect the mRNA expression levels of fiber markers and inflammatory markers, and Western blot was used to detect the related protein expression level of TGF -β/ Smad signaling pathway cells in each group.【Results】 Compared with TGF- β1 group, fiber markers(α- SMA mRNA, Collagen-ⅠmRNA and CTGF mRNA) inflammatory marker (IL-1βmRNA, IL-6 mRNA and TNF- αmRNA) and TGF-β/ Smad signaling pathway related proteins (p-Smad2, p-smad3) of the AG group, the PFD group and the AG + PFD group were significantly down regulated (mean P<0.05); Compared with the PFD group, the expression levels of α- SMA mRNA and IL-6 mRNA in the AG + PFD group were significantly down regulated (mean P<0.05).【Conclusion】 Compared with monotherapy, AG combined with PFD therapy has significant effect on the activation of hepatic stellate cells induced by TGF-β1, and plays a better role in anti hepatic fibrosis, and its mechanism may be related to the regulation of TGF-β/ Smad signaling pathway.

Key words： Liver/CY Astrocytes Transforming Growth Factor beta1 Pyridones ANDROGRAPHOLIDE

Received: 10 January 2022

PACS:

R322.47

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors

Cite this article:

URL:

http://journal07.magtech.org.cn/yxlcyj/EN/10.3969/j.issn.1671-7171.2022.02.003 OR http://journal07.magtech.org.cn/yxlcyj/EN/Y2022/V39/I2/168

[1] NETO J S, FEIER F H, BIERRENBACH A L, et al. Impact of Kasai portoenterostomy on liver transplantation outcomes: A retrospective cohort study of 347 children with biliary atresia[J].Liver Transpl,2015, 21(7): 922-927.
[2] 吴晓霞, 任红霞, 靳园园, 等. 胆道闭锁Kasai手术后自体肝生存时间小于2年的危险因素分析[J].临床小儿外科杂志, 2021, 20(2): 114-118.
[3] 许杜娟, 刘萌芽, 刘改枝, 等. 穿心莲内酯新剂型研究进展[J].中国新药杂志, 2021, 30(13): 1207-1212.
[4] LANCASTER L H, DE ANDRADE J A, ZIBRAK J D, et al.Pirfenidone safety and adverse event management in idiopathic pulmonary fibrosis [J].Eur Respir Rev,2017, 26(146):170057.
[5] 谢婧, 李丽华. 脱水穿心莲内酯对四氯化碳诱导的肝纤维化模型小鼠肝细胞凋亡的抑制作用及其机制[J].吉林大学学报(医学版), 2019, 45(5):1009-1014.
[6] VERMA N, KUMAR P, MITRA S, et al. Drug idiosyncrasy due to pirfenidone presenting as acute liver failure: Case report and mini-review of the literature [J].Hepatol Commun,2017, 2(2):142-147.
[7] KUMAR S, WANG J, SHANMUKHAPPA S K, et al. Toll-like receptor 4-independent carbon tetrachloride-induced fibrosis and lipopolysaccharide-induced acute liver injury in mice: role of hepatic stellate cells [J].Am J Pathol,2017, 187(6): 1356-1367.
[8] 汪俊祥, 蒲思宇, 王琦, 等. 核转录因子Gli在胆道闭锁肝上皮间充质转化中的调控作用[J].中华小儿外科杂志, 2021, 42(9): 823-829.
[9] 李万福, 李朝旺, 梁挺, 等. 转化生长因子-β1、结缔组织生长因子与胆道闭锁患儿肝硬化程度相关性研究[J].新疆医科大学学报, 2015, 38(11):1367-1371.
[10] 孙雪, 任红霞. 胆道闭锁发生与肝纤维化的分子机制研究进展[J].临床小儿外科杂志, 2019, 18(5): 432-436.
[11] 阿里木江·阿不都热依木, 林峰, 王皓洁, 等. Notch信号通路活化协同巨噬细胞对胆道闭锁肝纤维化的作用研究[J].临床小儿外科杂志, 2021, 20(4): 376-381.
[12] LI F B, ZHAO H, PENG K R, et al. Expression of transforming growth factor-β1 and connective tissue growth factor in congenital biliary atresia and neonatal hepatitis liver tissue [J].Genet Mol Res,2016,15(1):1-9.
[13] XU F, LIU C, ZHOU D, et al. TGF-β/SMAD Pathway and Its Regulation in Hepatic Fibrosis [J].J Histochem Cytochem,2016, 64(3):157-167.
[14] 丁美云, 詹江华. 胆道闭锁肝纤维化研究进展[J].天津医药, 2015, 43(1):4-7.

[1]	. [J]. JOURNAL OF CLINICAL RESEARCH, 2021, 38(10): 1441-1444.