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Quercetin prevents pyrrolizidine alkaloid clivorine-induced liver injury in mice by elevating body defense capacity.

Ji L, Ma Y, Wang Z, Cai Z, Pang C, Wang Z - PLoS ONE (2014)

Bottom Line: Results also showed that quercetin reduced the increase in liver glutathione and lipid peroxidative product malondialdehyde induced by clivorine.Quercetin reduced the enhanced liver immunohistochemical staining for 4-hydroxynonenal induced by clivorine.Some of the alterations were confirmed by real-time PCR.

View Article: PubMed Central - PubMed

Affiliation: The MOE Key Laboratory for Standardization of Chinese Medicines, The SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese Medicines and Shanghai Key Laboratory of Complex Prescription, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China; Shanghai R&D Centre for Standardization of Chinese Medicines, Shanghai, China.

ABSTRACT
Quercetin is a plant-derived flavonoid that is widely distributed in nature. The present study is designed to analyze the underlying mechanism in the protection of quercetin against pyrrolizidine alkaloid clivorine-induced acute liver injury in vivo. Serum transaminases, total bilirubin analysis, and liver histological evaluation demonstrated the protection of quercetin against clivorine-induced liver injury. Terminal dUTP nick end-labeling assay demonstrated that quercetin reduced the increased amount of liver apoptotic cells induced by clivorine. Western-blot analysis of caspase-3 showed that quercetin inhibited the cleaved activation of caspase-3 induced by clivorine. Results also showed that quercetin reduced the increase in liver glutathione and lipid peroxidative product malondialdehyde induced by clivorine. Quercetin reduced the enhanced liver immunohistochemical staining for 4-hydroxynonenal induced by clivorine. Results of the Mouse Stress and Toxicity PathwayFinder RT2 Profiler PCR Array demonstrated that the expression of genes related with oxidative or metabolic stress and heat shock was obviously altered after quercetin treatment. Some of the alterations were confirmed by real-time PCR. Our results demonstrated that quercetin prevents clivorine-induced acute liver injury in vivo by inhibiting apoptotic cell death and ameliorating oxidative stress injury. This protection may be caused by the elevation of the body defense capacity induced by quercetin.

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Expression profile of 84 genes included in the Stress and Toxicity PathwayFinder PCR Array in control and quercetin-treated mice.(A) The layout of the genes included in the Stress and Toxicity PathwayFinder PCR Array. (B) Heat map of the variations in the expression of 84 genes between control and quercetin-treated mice are shown as a fold increase or decrease.
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pone-0098970-g007: Expression profile of 84 genes included in the Stress and Toxicity PathwayFinder PCR Array in control and quercetin-treated mice.(A) The layout of the genes included in the Stress and Toxicity PathwayFinder PCR Array. (B) Heat map of the variations in the expression of 84 genes between control and quercetin-treated mice are shown as a fold increase or decrease.

Mentions: The layout of the genes of PCR array is shown in Fig. 7A, and Fig. 7B is a heat map that shows the fold regulation expression data between quercetin (90 mg/kg) and the control group. Numerous red and purple data are shown in Fig. 7B, which indicates that the expression of such genes was up-regulated in the livers of quercetin-treated mice. The differentially expressed genes over 5-folds between control and quercetin-treated group are listed in Table 1. Fmo5, Polr2k, Sod2, Ephx2, Sod1, Hmox2, and Hmox1 belong to the family of oxidative stress. Cyp2b10, Cyp1b1, Cyp2a5, Cyp3a11, and Cyp7a1 belong to the family of metabolic stress. Hspa5, Hspa1l, Hspa1b, Dnaja1, and Hspe1 belong to the family of heat shock.


Quercetin prevents pyrrolizidine alkaloid clivorine-induced liver injury in mice by elevating body defense capacity.

Ji L, Ma Y, Wang Z, Cai Z, Pang C, Wang Z - PLoS ONE (2014)

Expression profile of 84 genes included in the Stress and Toxicity PathwayFinder PCR Array in control and quercetin-treated mice.(A) The layout of the genes included in the Stress and Toxicity PathwayFinder PCR Array. (B) Heat map of the variations in the expression of 84 genes between control and quercetin-treated mice are shown as a fold increase or decrease.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4048295&req=5

pone-0098970-g007: Expression profile of 84 genes included in the Stress and Toxicity PathwayFinder PCR Array in control and quercetin-treated mice.(A) The layout of the genes included in the Stress and Toxicity PathwayFinder PCR Array. (B) Heat map of the variations in the expression of 84 genes between control and quercetin-treated mice are shown as a fold increase or decrease.
Mentions: The layout of the genes of PCR array is shown in Fig. 7A, and Fig. 7B is a heat map that shows the fold regulation expression data between quercetin (90 mg/kg) and the control group. Numerous red and purple data are shown in Fig. 7B, which indicates that the expression of such genes was up-regulated in the livers of quercetin-treated mice. The differentially expressed genes over 5-folds between control and quercetin-treated group are listed in Table 1. Fmo5, Polr2k, Sod2, Ephx2, Sod1, Hmox2, and Hmox1 belong to the family of oxidative stress. Cyp2b10, Cyp1b1, Cyp2a5, Cyp3a11, and Cyp7a1 belong to the family of metabolic stress. Hspa5, Hspa1l, Hspa1b, Dnaja1, and Hspe1 belong to the family of heat shock.

Bottom Line: Results also showed that quercetin reduced the increase in liver glutathione and lipid peroxidative product malondialdehyde induced by clivorine.Quercetin reduced the enhanced liver immunohistochemical staining for 4-hydroxynonenal induced by clivorine.Some of the alterations were confirmed by real-time PCR.

View Article: PubMed Central - PubMed

Affiliation: The MOE Key Laboratory for Standardization of Chinese Medicines, The SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese Medicines and Shanghai Key Laboratory of Complex Prescription, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China; Shanghai R&D Centre for Standardization of Chinese Medicines, Shanghai, China.

ABSTRACT
Quercetin is a plant-derived flavonoid that is widely distributed in nature. The present study is designed to analyze the underlying mechanism in the protection of quercetin against pyrrolizidine alkaloid clivorine-induced acute liver injury in vivo. Serum transaminases, total bilirubin analysis, and liver histological evaluation demonstrated the protection of quercetin against clivorine-induced liver injury. Terminal dUTP nick end-labeling assay demonstrated that quercetin reduced the increased amount of liver apoptotic cells induced by clivorine. Western-blot analysis of caspase-3 showed that quercetin inhibited the cleaved activation of caspase-3 induced by clivorine. Results also showed that quercetin reduced the increase in liver glutathione and lipid peroxidative product malondialdehyde induced by clivorine. Quercetin reduced the enhanced liver immunohistochemical staining for 4-hydroxynonenal induced by clivorine. Results of the Mouse Stress and Toxicity PathwayFinder RT2 Profiler PCR Array demonstrated that the expression of genes related with oxidative or metabolic stress and heat shock was obviously altered after quercetin treatment. Some of the alterations were confirmed by real-time PCR. Our results demonstrated that quercetin prevents clivorine-induced acute liver injury in vivo by inhibiting apoptotic cell death and ameliorating oxidative stress injury. This protection may be caused by the elevation of the body defense capacity induced by quercetin.

Show MeSH
Related in: MedlinePlus