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Article: Integrating Network Pharmacology and Experimental Models to Investigate the Efficacy of Coptidis and Scutellaria Containing Huanglian Jiedu Decoction on Hepatocellular Carcinoma

TitleIntegrating Network Pharmacology and Experimental Models to Investigate the Efficacy of Coptidis and Scutellaria Containing Huanglian Jiedu Decoction on Hepatocellular Carcinoma
Authors
KeywordsCoxsackievirus B3
Baicalin
Lipid Synthesis
Autophagosome
Issue Date2020
PublisherWorld Scientific Publishing Co Pte Ltd. The Journal's web site is located at http://www.worldscinet.com/ajcm/ajcm.shtml
Citation
The American Journal of Chinese Medicine, 2020, v. 48 n. 1, p. 161-182 How to Cite?
AbstractBaicalin is a flavonoid extracted from Scutellariae Radix and shows a variety of biological activities as reducing lipids, diminishing inflammation, and inhibiting bacterial infection. However, there is no report of baicalin against CVB3 infection. In this study, we found that baicalin can reduce viral titer in a dose-dependent manner in vitro at a dose with no direct virucidal effect. Moreover, we revealed that baicalin can also improve survival rate, reduce heart weight/body weight ratio, prevent virus replication, and relieve myocardial inflammation in the acute viral myocarditis mouse model induced by CVB3. Then, in order to explore the mechanism of baicalin inhibiting CVB3 replication, we respectively examined the expression of autophagosome marker LC3-II by Western blot, tested the concentration of free fatty acid (FFA) and cholesterol (CHO) by commercial kits, detected the mRNA levels of fatty acid synthase (Fasn) and acetyl coenzyme a carboxylase (ACC) by RT-PCR, and observed the lipid content of cells by fluorescence staining. The results showed that CVB3 infection increased autophagosome formation and lipid content in HeLa cells, but these changes were significantly blocked by baicalin. Finally, in order to confirm that baicalin inhibits viral replication and reduces autophagosome formation by reducing cellular lipids, we added exogenous palmitate to cell culture supernatants to promote intracellular lipid synthesis and found that palmitate did not alter LC3-II and CVB3/VP1 expression in HeLa cells with or without CVB3 infection. Interestingly, palmitate can reverse the inhibitory effect of baicalin on autophagosome formation and viral replication. In conclusion, our results indicated that lipids play an important role in CVB3 replication, and the effect of baicalin against CVB3 was associated with its ability to reduce cellular lipid synthesis to limit autophagosome formation.
Persistent Identifierhttp://hdl.handle.net/10722/282260
ISSN
2020 Impact Factor: 4.667
2015 SCImago Journal Rankings: 0.797
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHuang, J-
dc.contributor.authorGuo, W-
dc.contributor.authorCheung, F-
dc.contributor.authorTan, HY-
dc.contributor.authorWang, N-
dc.contributor.authorFeng, Y-
dc.date.accessioned2020-05-05T14:32:50Z-
dc.date.available2020-05-05T14:32:50Z-
dc.date.issued2020-
dc.identifier.citationThe American Journal of Chinese Medicine, 2020, v. 48 n. 1, p. 161-182-
dc.identifier.issn0192-415X-
dc.identifier.urihttp://hdl.handle.net/10722/282260-
dc.description.abstractBaicalin is a flavonoid extracted from Scutellariae Radix and shows a variety of biological activities as reducing lipids, diminishing inflammation, and inhibiting bacterial infection. However, there is no report of baicalin against CVB3 infection. In this study, we found that baicalin can reduce viral titer in a dose-dependent manner in vitro at a dose with no direct virucidal effect. Moreover, we revealed that baicalin can also improve survival rate, reduce heart weight/body weight ratio, prevent virus replication, and relieve myocardial inflammation in the acute viral myocarditis mouse model induced by CVB3. Then, in order to explore the mechanism of baicalin inhibiting CVB3 replication, we respectively examined the expression of autophagosome marker LC3-II by Western blot, tested the concentration of free fatty acid (FFA) and cholesterol (CHO) by commercial kits, detected the mRNA levels of fatty acid synthase (Fasn) and acetyl coenzyme a carboxylase (ACC) by RT-PCR, and observed the lipid content of cells by fluorescence staining. The results showed that CVB3 infection increased autophagosome formation and lipid content in HeLa cells, but these changes were significantly blocked by baicalin. Finally, in order to confirm that baicalin inhibits viral replication and reduces autophagosome formation by reducing cellular lipids, we added exogenous palmitate to cell culture supernatants to promote intracellular lipid synthesis and found that palmitate did not alter LC3-II and CVB3/VP1 expression in HeLa cells with or without CVB3 infection. Interestingly, palmitate can reverse the inhibitory effect of baicalin on autophagosome formation and viral replication. In conclusion, our results indicated that lipids play an important role in CVB3 replication, and the effect of baicalin against CVB3 was associated with its ability to reduce cellular lipid synthesis to limit autophagosome formation.-
dc.languageeng-
dc.publisherWorld Scientific Publishing Co Pte Ltd. The Journal's web site is located at http://www.worldscinet.com/ajcm/ajcm.shtml-
dc.relation.ispartofThe American Journal of Chinese Medicine-
dc.rightsElectronic version of an article published as The American Journal of Chinese Medicine, 2020, v. 48 n. 1, p. 161-182. DOI: 10.1142/S0192415X20500093 © World Scientific Publishing Company [https://www.worldscientific.com/doi/abs/10.1142/S0192415X20500093]-
dc.subjectCoxsackievirus B3-
dc.subjectBaicalin-
dc.subjectLipid Synthesis-
dc.subjectAutophagosome-
dc.titleIntegrating Network Pharmacology and Experimental Models to Investigate the Efficacy of Coptidis and Scutellaria Containing Huanglian Jiedu Decoction on Hepatocellular Carcinoma-
dc.typeArticle-
dc.identifier.emailTan, HY: hyhtan@hku.hk-
dc.identifier.emailWang, N: ckwang@hku.hk-
dc.identifier.emailFeng, Y: yfeng@hku.hk-
dc.identifier.authorityWang, N=rp02075-
dc.identifier.authorityFeng, Y=rp00466-
dc.description.naturepostprint-
dc.identifier.doi10.1142/S0192415X20500093-
dc.identifier.pmid31964157-
dc.identifier.scopuseid_2-s2.0-85078346210-
dc.identifier.hkuros309780-
dc.identifier.volume48-
dc.identifier.issue1-
dc.identifier.spage161-
dc.identifier.epage182-
dc.identifier.isiWOS:000515156400009-
dc.publisher.placeSingapore-
dc.identifier.issnl0192-415X-

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