Hepatic oxidative stress in ovariectomized transgenic mice expressing the hepatitis <scp>C</scp> virus polyprotein is augmented through suppression of adenosine monophosphate‐activated protein kinase/proliferator‐activated receptor gamma co‐activator 1 alpha signaling

Tomiyama, Yasuyuki; Nishina, Sohji; Hara, Yuichi; Kawase, Tomoya; Hino, Keisuke

doi:10.1111/hepr.12254

Cited by 3 publications

(3 citation statements)

References 38 publications

(71 reference statements)

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“…overcome the detrimental oxidative stress associated with ovariectomy by decreasing the levels of hepatic MDA and increasing the levels of the hepatic total glutathione. Menopause can induce abnormal serum lipid production, substantially affecting liver function, causing excessive production of reactive oxygen species (ROS), starting lipid peroxidation, impairing liver function, and adversely affecting the cardiovascular system [2,8,29]. Hepatocyte possesses an enzyme system to protect against oxidative stress, and regulating endogenous antioxidants in the liver not only prevents fatty liver production but also prevents the onset of cardiovascular disease.…”

Section: Discussionmentioning

confidence: 99%

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Improvement in Menopause‐Associated Hepatic Lipid Metabolic Disorders by Herbal Formula HPC03 on Ovariectomized Rats

Chang

Kim

2020

Evidence-Based Complementary and Alternative Medicine

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Postmenopausal women have an increased risk of developing nonalcoholic fatty liver disease (NAFLD). We formulated a combination of three herb mixtures (HPC03) and observed lipid-lowering efficacy. HepG2 cells were treated with oleic acid to induce an NAFLD model (in vitro). Also, we investigated potential of HPC03 in an ovariectomize- (OVX-) induced NAFLD model (in vivo). We separated the mice into six groups, as follows: SHAM, OVX, OVX + β-estradiol, and OVX + HPC03 (50, 100, and 200 mg/kg). Rats were administered with/without HPC03 for 12 weeks. HPC03 dose dependently inhibited the lipid accumulation involved in lipogenesis in HepG2 cells. The body weight, fat mass, and weights of the liver were decreased in the OVX group than that in the other groups. HPC03 had decreased adiposity that was induced by OVX. HPC03 treatment reduced liver lipid deposition and prevented the increase in serum and liver triglyceride export when there was a deficiency in estradiol. HPC03 improves OVX-induced fatty liver and lipid metabolism. These findings suggest that HPC03 from postmenopausal women has a protective effect during NAFLD conditions.

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Section: Discussionmentioning

confidence: 99%

“…For studies related to postmenopausal women, natural menopausal animal models and artificially ovariectomized models are used. Among them, ovariectomized models are more commonly used [ 28 , 29 ]. Several studies have also shown that estrogen receptor alpha (ER α ) is associated with weight control and lipid accumulation [ 7 , 30 ].…”

Section: Discussionmentioning

confidence: 99%

Improvement in Menopause‐Associated Hepatic Lipid Metabolic Disorders by Herbal Formula HPC03 on Ovariectomized Rats

Chang

Kim

2020

Evidence-Based Complementary and Alternative Medicine

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“…There are several markers for evaluating oxidative stress, including 8-hydroxyguanosine, 4-hydroxynonenal protein, and activity of glutathione and superoxide dismutase (35,36). Additionally, the levels of d-ROM and BAP have been used to evaluate oxidative status.…”

Section: Discussionmentioning

confidence: 99%

Wheat-bran autolytic peptides containing a branched-chain amino acid attenuate non-alcoholic steatohepatitis via the suppression of oxidative stress and the upregulation of AMPK/ACC in high-fat diet-fed mice

Kawaguchi

Ueno

Nogata

et al. 2016

International Journal of Molecular Medicine

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Abstract. Whole-wheat intake is known to reduce the risk of metabolic syndrome. However, the active component remains unclear. Recently, we identified bioactive peptides [leucinearginine-proline (LRP) and leucine-glutamine-proline (LQP)] from wheat bran autolytic hydrolysate. The present study aimed to investigate the effects of LRP and LQP on non-alcoholic steatohepatitis (NASH) in a mouse model. We also evaluated the effects of these peptides on oxidative stress and on the AMP-activated protein kinase (AMPK) signaling pathway, two major pathogenic factors of NASH. Seven-week-old male C57BL/6 mice were fed a high-fat diet for 10 weeks and administered water supplemented with 0.05% LRP, 0.20% LRP, 0.05% LQP, or 0.20% LQP (each n=5) or distilled water (control; n=5) ad libitum. Oxidative stress was evaluated by measuring the serum levels of diacron reactive oxygen metabolite (d-ROM) and biological antioxidant potential (BAP). Hepatic expression of phosphorylated AMPK and phosphorylated acetyl-CoA carboxylase (ACC) were evaluated by immunoblotting. The result showed that non-alcoholic fatty liver disease activity score was significantly decreased in all types of treatment. Serum d-ROM levels were significantly decreased in the 0.20% LRP group, but not in the 0.05% LRP, 0.05% LQP, and 0.20% LQP groups. Serum BAP levels were significantly increased in the 0.05% LRP and 0.20% LRP groups, but not in the 0.05% LQP and 0.20% LQP groups. Immunoblotting analysis revealed that the expression of phospho-AMPK was increased whereas that of phospho-ACC was decreased in the 0.20% LQP group. In conclusion, we demonstrated that both LRP and LQP alleviated the severity of NASH in a high-fat diet-induced NASH mouse model. In addition, we showed that LRP and LQP modulated oxidative stress and upregulated AMPK/ACC, respectively. Thus, LRP and LQP may constitute clinically applicable therapeutic agents for NASH. IntroductionNon-alcoholic fatty liver disease (NAFLD) is a hepatic manifestation of metabolic syndrome. The prevalence of NAFLD is estimated to range from 25 to 37% of the general population (1-4), and it constitutes a common etiological factor of chronic liver disease worldwide. Non-alcoholic steatohepatitis (NASH) is a progressive form of NAFLD. Patients with NASH have a high risk of life-threatening complications, including cardiovascular disease, liver cirrhosis, and hepatocellular carcinoma (5,6). In addition, NASH is predicted to become the leading cause of liver transplantation in the USA by the year 2020 (2). Thus, NAFLD/NASH is becoming a major social issue worldwide.The first-line therapy for NASH is life-style intervention. Although diet and exercise alleviate the severity of NASH, long-term adherence to life-style interventions is poor (7,8). Pioglitazone, an insulin-sensitizing anti-diabetic agent, leads to metabolic and histologic improvement in patients with NASH (9). However, the indication of pioglitazone is restricted to NASH patients with diabetes mellitus (10). Furthermore, severe liver disease is a contrai...

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Natural mineral-rich water ingestion by ovariectomized fructose-fed Sprague-Dawley rats: effects on sirtuin 1 and glucocorticoid signaling pathways

et al. 2017

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Hepatic oxidative stress in ovariectomized transgenic mice expressing the hepatitis C virus polyprotein is augmented through suppression of adenosine monophosphate‐activated protein kinase/proliferator‐activated receptor gamma co‐activator 1 alpha signaling

Cited by 3 publications

References 38 publications

Improvement in Menopause‐Associated Hepatic Lipid Metabolic Disorders by Herbal Formula HPC03 on Ovariectomized Rats

Improvement in Menopause‐Associated Hepatic Lipid Metabolic Disorders by Herbal Formula HPC03 on Ovariectomized Rats

Wheat-bran autolytic peptides containing a branched-chain amino acid attenuate non-alcoholic steatohepatitis via the suppression of oxidative stress and the upregulation of AMPK/ACC in high-fat diet-fed mice

Natural mineral-rich water ingestion by ovariectomized fructose-fed Sprague-Dawley rats: effects on sirtuin 1 and glucocorticoid signaling pathways

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