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Protective effect of bicyclol on tetracycline-induced fatty liver in mice.
Toxicology. 2009 Jul 10; 261(3):112-8.T

Abstract

Peroxisome proliferators-activated receptor alpha (PPARalpha) and oxidative stress are two important pathological factors in non-alcoholic fatty liver disease (NAFLD). Tetracycline-induced fatty liver was partly due to the disturbance of mitochondrial fatty acids beta-oxidation regulated by PPARalpha. Bicyclol was found to protect against high fat diet-induced fatty liver through modulating PPARalpha and clearing reactive oxygen species (ROS). The present study was performed to further investigate the effect of bicyclol on tetracycline-induced fatty liver and related mechanism in mice. Bicyclol (75, 150, 300 mg/kg) was given orally three times in two consecutive days. Tetracycline (200 mg/kg) was injected intraperitoneally 1h after the last administration of bicyclol. Oxidative stress, mitochondrial function, PPARalpha and its target genes were evaluated by biochemical and RT-PCR analysis. The activity of CYP4A was assessed by liquid chromatography/mass spectrometry (LC/MS) method. Bicyclol significantly protected against tetracycline-induced fatty liver by reducing the accumulation of hepatic lipids and elevation of serum aminotransferase. In addition, bicyclol remarkably alleviated the over-production of thiobarbituric acid-reactive substance. The reduced activity of mitochondrial respiratory chain (MRC) complexes I and IV and mitochondrial permeability transition (MPT) were also improved by bicyclol. Furthermore, bicyclol inhibited the decrease of PPARalpha expression and its target genes, including long-chain acyl CoA dehydrogenase (LCAD), acetyl CoA oxidase (AOX) and CYP4A at mRNA and enzyme activity level. Bicyclol protected against tetracycline-induced fatty liver mainly through modulating the disturbance of PPARalpha pathway and ameliorating mitochondrial function.

Authors+Show Affiliations

Department of New Drug Development, Institute of Materia Medica, Peking Union Medical College, [corrected] Chinese Academy of Medical Sciences, No. 1, Xian Nong Tan Street, Beijing 100050, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19427351

Citation

Yu, Hong-Yan, et al. "Protective Effect of Bicyclol On Tetracycline-induced Fatty Liver in Mice." Toxicology, vol. 261, no. 3, 2009, pp. 112-8.
Yu HY, Wang BL, Zhao J, et al. Protective effect of bicyclol on tetracycline-induced fatty liver in mice. Toxicology. 2009;261(3):112-8.
Yu, H. Y., Wang, B. L., Zhao, J., Yao, X. M., Gu, Y., & Li, Y. (2009). Protective effect of bicyclol on tetracycline-induced fatty liver in mice. Toxicology, 261(3), 112-8. https://doi.org/10.1016/j.tox.2009.04.058
Yu HY, et al. Protective Effect of Bicyclol On Tetracycline-induced Fatty Liver in Mice. Toxicology. 2009 Jul 10;261(3):112-8. PubMed PMID: 19427351.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protective effect of bicyclol on tetracycline-induced fatty liver in mice. AU - Yu,Hong-Yan, AU - Wang,Bao-Lian, AU - Zhao,Jing, AU - Yao,Xiao-Min, AU - Gu,Yu, AU - Li,Yan, Y1 - 2009/05/07/ PY - 2009/02/23/received PY - 2009/04/10/revised PY - 2009/04/29/accepted PY - 2009/5/12/entrez PY - 2009/5/12/pubmed PY - 2009/7/10/medline SP - 112 EP - 8 JF - Toxicology JO - Toxicology VL - 261 IS - 3 N2 - Peroxisome proliferators-activated receptor alpha (PPARalpha) and oxidative stress are two important pathological factors in non-alcoholic fatty liver disease (NAFLD). Tetracycline-induced fatty liver was partly due to the disturbance of mitochondrial fatty acids beta-oxidation regulated by PPARalpha. Bicyclol was found to protect against high fat diet-induced fatty liver through modulating PPARalpha and clearing reactive oxygen species (ROS). The present study was performed to further investigate the effect of bicyclol on tetracycline-induced fatty liver and related mechanism in mice. Bicyclol (75, 150, 300 mg/kg) was given orally three times in two consecutive days. Tetracycline (200 mg/kg) was injected intraperitoneally 1h after the last administration of bicyclol. Oxidative stress, mitochondrial function, PPARalpha and its target genes were evaluated by biochemical and RT-PCR analysis. The activity of CYP4A was assessed by liquid chromatography/mass spectrometry (LC/MS) method. Bicyclol significantly protected against tetracycline-induced fatty liver by reducing the accumulation of hepatic lipids and elevation of serum aminotransferase. In addition, bicyclol remarkably alleviated the over-production of thiobarbituric acid-reactive substance. The reduced activity of mitochondrial respiratory chain (MRC) complexes I and IV and mitochondrial permeability transition (MPT) were also improved by bicyclol. Furthermore, bicyclol inhibited the decrease of PPARalpha expression and its target genes, including long-chain acyl CoA dehydrogenase (LCAD), acetyl CoA oxidase (AOX) and CYP4A at mRNA and enzyme activity level. Bicyclol protected against tetracycline-induced fatty liver mainly through modulating the disturbance of PPARalpha pathway and ameliorating mitochondrial function. SN - 1879-3185 UR - https://www.unboundmedicine.com/medline/citation/19427351/Protective_effect_of_bicyclol_on_tetracycline_induced_fatty_liver_in_mice_ DB - PRIME DP - Unbound Medicine ER -