Correlation between oxidative stress and Hydroxyproline content in Liver Fibrosis

Oxidative stress plays a pivotal role in the progression of chronic hepatitis B; however, it is unclear whether the status of blood oxidative stress and antioxidant components differs depending on the degree of hepatic fibrosis. To explore the relationship between oxidative stress/antioxidant capacity and the extent of hepatic fibrosis, fifty-four subjects with liver fibrosis (5.5 ≤ liver stiffness measurement (LSM) score ≤ 16.0 kPa) by chronic hepatitis B virus (HBV) were analyzed. From the analysis of eight kinds of serum oxidative stress/antioxidant profiles and liver fibrosis degrees, the level of total antioxidant capacity (TAC) reflected a negative correlation with the severity of hepatic fibrosis (Pearson correlation, r = −0.35, p = 0.01). Moreover, TAC showed higher sensitivity (73.91%) than the aspartate transaminase (AST) to platelet ratio index (APRI, 56.52%) in the receiver operating characteristic (ROC) curves. Interestingly, the TAC level finely reflected the fibrosis degree in inactive carriers (HBV DNA < 2000 IU/mL), while the APRI did in active carriers (HBV DNA > 2000 IU/mL). In conclusion, TAC is a promising biomarker for evaluating the progression of liver fibrosis in patients with HBV, and this finding may indicate the involvement of TAC-composing factors in the pathogenesis of hepatic fibrosis in chronic HBV carriers.

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Creatine Alleviates Doxorubicin-Induced Liver Damage by Inhibiting Liver Fibrosis, Inflammation, Oxidative Stress, and Cellular Senescence

Nutrients ◽

10.3390/nu13010041 ◽

2020 ◽

Vol 13 (1) ◽

pp. 41

Author(s):

Nouf Aljobaily ◽

Michael J. Viereckl ◽

David S. Hydock ◽

Hend Aljobaily ◽

Tsung-Yen Wu ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Methylation ◽

Body Weight ◽

Liver Fibrosis ◽

Liver Damage ◽

Cellular Senescence ◽

Weight Ratio ◽

Mrna Levels ◽

Body Weight Ratio ◽

Chromosomal Stability

Background: Treatment with the chemotherapy drug doxorubicin (DOX) may lead to toxicities that affect non-cancer cells including the liver. Supplementing the diet with creatine (Cr) has been suggested as a potential intervention to minimize DOX-induced side effects, but its effect in alleviating DOX-induced hepatoxicity is currently unknown. Therefore, we aimed to examine the effects of Cr supplementation on DOX-induced liver damage. Methods: Male Sprague-Dawley rats were fed a diet supplemented with 2% Cr for four weeks, 4% Cr for one week followed by 2% Cr for three more weeks, or control diet for four weeks. Animals then received either a bolus i.p. injection of DOX (15 mg/kg) or saline as a placebo. Animals were then sacrificed five days-post injection and markers of hepatoxicity were analyzed using the liver-to-body weight ratio, aspartate transaminase (AST)-to- alanine aminotransferase (ALT) ratio, alkaline phosphatase (ALP), lipemia, and T-Bilirubin. In addition, hematoxylin and eosin (H&E) staining, Picro-Sirius Red staining, and immunofluorescence staining for CD45, 8-OHdG, and β-galactosidase were performed to evaluate liver morphology, fibrosis, inflammation, oxidative stress, and cellular senescence, respectively. The mRNA levels for biomarkers of liver fibrosis, inflammation, oxidative stress, and senescence-related genes were measured in liver tissues. Chromosomal stability was evaluated using global DNA methylation ELISA. Results: The ALT/AST ratio and liver to body weight ratio tended to increase in the DOX group, and Cr supplementation tended to attenuate this increase. Furthermore, elevated levels of liver fibrosis, inflammation, oxidative stress, and senescence were observed with DOX treatment, and Cr supplementation prior to DOX treatment ameliorated this hepatoxicity. Moreover, DOX treatment resulted in chromosomal instability (i.e., altered DNA methylation profile), and Cr supplementation showed a tendency to restore chromosomal stability with DOX treatment. Conclusion: The data suggest that Cr protected against DOX-induced hepatotoxicity by attenuating fibrosis, inflammation, oxidative stress, and senescence.

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Apigenin protects mice against 3,5-diethoxycarbonyl-1,4-dihydrocollidine-induced cholestasis

Food & Function ◽

10.1039/d0fo02910f ◽

2021 ◽

Vol 12 (5) ◽

pp. 2323-2334

Author(s):

Shihong Zheng ◽

Peichang Cao ◽

Zequn Yin ◽

Xuerui Wang ◽

Yuanli Chen ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Metabolism ◽

Liver Fibrosis ◽

Liver Damage ◽

Liver Diseases ◽

Potential Drug ◽

Abnormal Lipid Metabolism ◽

And Oxidative Stress

Apigenin prevented the DDC-induced abnormal lipid metabolism, liver damage and liver fibrosis by reducing inflammation and oxidative stress. Apigenin might be a potential drug for the treatment of cholestatic liver diseases.

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Ameliorating effects of white mulberry on iron-overload-induced oxidative stress and liver fibrosis in Swiss albino mice

Food and Chemical Toxicology ◽

10.1016/j.fct.2021.112520 ◽

2021 ◽

pp. 112520

Author(s):

Anil Khushalrao Shendge ◽

Sourav Panja ◽

Tapasree Basu ◽

Nikhil Baban Ghate ◽

Nripendranath Mandal

Keyword(s):

Oxidative Stress ◽

Liver Fibrosis ◽

Iron Overload ◽

Swiss Albino Mice ◽

Albino Mice ◽

White Mulberry

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Ameliorative Effects of Nilotinib on CCl4 Induced Liver Fibrosis Via Attenuation of RAGE/HMGB1 Gene Expression and Oxidative Stress in Rat

Chonnam Medical Journal ◽

10.4068/cmj.2017.53.2.118 ◽

2017 ◽

Vol 53 (2) ◽

pp. 118 ◽

Cited By ~ 13

Author(s):

Vahid Khanjarsim ◽

Jamshid Karimi ◽

Iraj Khodadadi ◽

Adel Mohammadalipour ◽

Mohammad Taghi Goodarzi ◽

...

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Liver Fibrosis ◽

And Oxidative Stress

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Genetic differences in oxidative stress and inflammatory responses to diet-induced obesity do not alter liver fibrosis in mice

Liver International ◽

10.1111/j.1478-3231.2009.02036.x ◽

2009 ◽

Vol 29 (8) ◽

pp. 1262-1272 ◽

Cited By ~ 20

Author(s):

Wing-Kin Syn ◽

Liu Yang ◽

Dian Jung Chiang ◽

Yue Qian ◽

Youngmi Jung ◽

...

Keyword(s):

Oxidative Stress ◽

Liver Fibrosis ◽

Inflammatory Responses ◽

Genetic Differences ◽

Diet Induced Obesity

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RAP-8 ameliorates liver fibrosis by modulating cell cycle and oxidative stress

Life Sciences ◽

10.1016/j.lfs.2019.04.037 ◽

2019 ◽

Vol 229 ◽

pp. 200-209 ◽

Cited By ~ 3

Author(s):

Hongjiao Xu ◽

Sihua Hong ◽

Zhibin Yan ◽

Qian Zhao ◽

Ying Shi ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Cycle ◽

Liver Fibrosis ◽

And Oxidative Stress

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Withaferin A Exerts Preventive Effect on Liver Fibrosis through Oxidative Stress Inhibition in a Sirtuin 3-Dependent Manner

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/2452848 ◽

2020 ◽

Vol 2020 ◽

pp. 1-17

Author(s):

Jingya Gu ◽

Chang Chen ◽

Jue Wang ◽

Tingting Chen ◽

Wenjuan Yao ◽

...

Keyword(s):

Oxidative Stress ◽

Liver Fibrosis ◽

Withaferin A ◽

Dependent Manner ◽

Sirtuin 3 ◽

Antifibrogenic Effect ◽

Antioxidant Effects ◽

Sirt3 Expression ◽

Bioactive Constituent

Sirtuin 3 (SIRT3) is a deacetylase involved in the development of many inflammation-related diseases including liver fibrosis. Withaferin A (WFA) is a bioactive constituent derived from the Withania somnifera plant, which has extensive pharmacological activities; however, little is known about the regulatory role of SIRT3 in the WFA-induced antifibrogenic effect. The current study is aimed at investigating the role of SIRT3 in WFA-induced antioxidant effects in liver fibrosis. Our study verified that WFA attenuated platelet-derived growth factor BB- (PDGF-BB-) induced liver fibrosis and promoted PDGF-BB-induced SIRT3 activity and expression in JS1 cells. SIRT3 silencing attenuated the antifibrogenic and antioxidant effects of WFA in activated JS1 cells. Moreover, WFA inhibited carbon tetrachloride- (CCl4-) induced liver injury, collagen deposition, and fibrosis; increased the SIRT3 expression; and suppressed the CCl4-induced oxidative stress in fibrotic livers of C57/BL6 mice. Furthermore, the antifibrogenic and antioxidant effects of WFA could be available in CCl4-induced WT (129S1/SvImJ) mice but were unavailable in CCl4-induced SIRT3 knockout (KO) mice. Our study suggested that WFA inhibited liver fibrosis through the inhibition of oxidative stress in a SIRT3-dependent manner. WFA could be a potential compound for the treatment of liver fibrosis.

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