Limits...
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.

Show MeSH

Related in: MedlinePlus

Validation of gene expression by real-time PCR analysis.The mRNA expression of (A) Fmo5, Polr2k, Sod2, Ephx2, Sod1, Hmox2, and Hmox1; (B) Cyp2b10, Cyp1b1, Cyp2a5, Cyp3a11, and Cyp7a1; and (C) Hspa5, Hspa1l, Hspa1b, Dnaja1, Hspe1. Data are expressed as means ± SEM (n = 6 to 8). *P<0.05, ***P<0.001 compared with the control.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4048295&req=5

pone-0098970-g008: Validation of gene expression by real-time PCR analysis.The mRNA expression of (A) Fmo5, Polr2k, Sod2, Ephx2, Sod1, Hmox2, and Hmox1; (B) Cyp2b10, Cyp1b1, Cyp2a5, Cyp3a11, and Cyp7a1; and (C) Hspa5, Hspa1l, Hspa1b, Dnaja1, Hspe1. Data are expressed as means ± SEM (n = 6 to 8). *P<0.05, ***P<0.001 compared with the control.

Mentions: The expression of Fmo5, Polr2k, Sod2, Ephx2, Sod1, Hmox2, and Hmox1 genes was up-regulated in the livers of the quercetin-treated mice, which further confirmed the previous results in the PCR array (P<0.001, P<0.05) (Fig. 8A). In addition, clivorine decreased the mRNA expression of Sod1, Hmox2, Fmo5, and Ephx2 (P<0.05, P<0.01), whereas quercetin (90 mg/kg) reversed the decreased expression of Hmox2 and Fmo5 (P<0.05). Clivorine increased the mRNA expression of Hmox1 (P<0.05), whereas quercetin (90 mg/kg) decreased such increase (P<0.05).


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)

Validation of gene expression by real-time PCR analysis.The mRNA expression of (A) Fmo5, Polr2k, Sod2, Ephx2, Sod1, Hmox2, and Hmox1; (B) Cyp2b10, Cyp1b1, Cyp2a5, Cyp3a11, and Cyp7a1; and (C) Hspa5, Hspa1l, Hspa1b, Dnaja1, Hspe1. Data are expressed as means ± SEM (n = 6 to 8). *P<0.05, ***P<0.001 compared with the control.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0098970-g008: Validation of gene expression by real-time PCR analysis.The mRNA expression of (A) Fmo5, Polr2k, Sod2, Ephx2, Sod1, Hmox2, and Hmox1; (B) Cyp2b10, Cyp1b1, Cyp2a5, Cyp3a11, and Cyp7a1; and (C) Hspa5, Hspa1l, Hspa1b, Dnaja1, Hspe1. Data are expressed as means ± SEM (n = 6 to 8). *P<0.05, ***P<0.001 compared with the control.
Mentions: The expression of Fmo5, Polr2k, Sod2, Ephx2, Sod1, Hmox2, and Hmox1 genes was up-regulated in the livers of the quercetin-treated mice, which further confirmed the previous results in the PCR array (P<0.001, P<0.05) (Fig. 8A). In addition, clivorine decreased the mRNA expression of Sod1, Hmox2, Fmo5, and Ephx2 (P<0.05, P<0.01), whereas quercetin (90 mg/kg) reversed the decreased expression of Hmox2 and Fmo5 (P<0.05). Clivorine increased the mRNA expression of Hmox1 (P<0.05), whereas quercetin (90 mg/kg) decreased such increase (P<0.05).

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