ABSTRACT
In the present study, we investigated the potential pathogenesis of coxsackievirus B3 (CVB3)-induced viral myocarditis and the promising protective effect of silencing RNA (small interfering RNA, siRNA). One hundred and twenty mice were included in the study, and 30 mice were intraperitoneally inoculated with CVB3 to establish an acute viral myocarditis model. The survival rate was observed for the CVB3-infected mouse model (MOD), and myocardial injury was examined by HE (hematoxylin and eosin) staining assay. Real-time PCR (RT-PCR) and Western blot assay were selected to detect the toll-like receptor 4 (TLR4) expression in myocardial tissues. The TLR4 gene was silenced for the MOD mice, and the effects of this treatment were observed. The results indicate that the expression of TLR4 mRNA and the protein significantly and persistently increased during the progression of CVB3-induced myocarditis. The activities of cardiac enzymes including CK, LDH, AST, and CK-MB were also enhanced in CVB3-induced myocardial tissues. Interestingly, when the TLR4 gene was silenced, the CVB3-induced TLR4 production was significantly decreased and the severity of myocarditis was significantly lessened. In conclusion, CVB3 may induce viral myocarditis by upregulating toll-like receptor 4 expression. The viral myocarditis can be ameliorated by silencing the TLR4 gene in the CVB3 viral myocarditis model, which may be a feasible therapeutic method for treatment of viral myocarditis.
Subject(s)
Coxsackievirus Infections/genetics , Enterovirus B, Human , Myocarditis/genetics , Toll-Like Receptor 4/genetics , Up-Regulation , Animals , Coxsackievirus Infections/metabolism , Coxsackievirus Infections/virology , Disease Models, Animal , Male , Mice , Myocarditis/metabolism , Myocarditis/virology , Myocardium/metabolism , Toll-Like Receptor 4/metabolismABSTRACT
Two new triterpenoid saponins acylated with monoterpenic acid, 2ß,23-dihydroxy-3-O-α-L-rhamnopyranosyl-21-O-{(6S)-2-trans-2,6-dimethyl-6-O-[3-O-(ß-D-glucopyranosyl)-4-O-(2-methylbutanoyl)-ß-L-arabinopyranosyl]-2,7-octadienoyl)-acacic acid 28-O-ß-D-xylopyranosyl-(1 â 3)-ß-D-xylopyranosyl-(1 â 4)-[ß-D-glucopyranosyl-(1 â 3)]-α-L-rhamnopyranosyl-(1 â 2)-[α-L-rhamnopyranosyl-(1 â 6)]-ß-D-glucopyranosyl ester and 2ß,23-dihydroxy-3-O-α-L-rhamnopyranosyl-21-O-{(6S)-2-trans-2,6-dimethyl-6-O-[4-O-((6S)-2-trans-2,6-dimethyl-6-O-(ß-L-arabinopyranosyl)-2,7-octadienoyl)]-ß-L-arabinopyranosyl]-2,7-octadienoyl}-acacic acid 28-O-ß-D-xylopyranosyl-(1 â 3)-ß-D-xylopyranosyl-(1 â 4)-[ß-D-glucopyranosyl-(1 â 3)]-α-L-rhamnopyranosyl-(1 â 2)-[α-L-rhamnopyranosyl-(1 â 6)]-ß-D-glucopyranosyl ester were isolated from the fruit of Gymnocladus chinensis Baill. and the structural elucidation of both the compounds was accomplished by extensive studies of their spectroscopic (1D and 2D NMR, TOF-MS, QFT-MS) and chemical methods.
Subject(s)
Fabaceae/chemistry , Saponins/chemistry , Triterpenes/chemistry , Molecular StructureABSTRACT
A new triterpenoid saponin acylated with monoterpenic acid, together with two known triterpenoid saponins, has been isolated from the fruit of Gymnocladus chinensis Baill. Their structures were elucidated as 2ß,23-dihydroxy-3-O-α-L-rhamnopyranosyl-21-O-{(6S)-2-trans-2,6-dimethyl-6-O-[3-O-(ß-D-glucopyranosyl)-4-O-((6S)-2-trans-2,6-dimethyl-6-hydroxy-2,7-octadienoyl)-ß-L-arabinopyranosyl]-2,7-octadienoyl}-acacic acid 28-O-ß-D-xylopyranosyl-(1 â 3)-ß-D-xylopyranosyl-(1 â 4)-α-L-rhamnopyranosyl-(1 â 2)-[α-L-rhamnopyranosyl-(1 â 6)]-ß-D-glucopyranosyl ester (1), gymnocladus saponin E (2), and gymnocladus saponin F(2) (3).