Endoplasmic Reticulum Stress Response in Non-alcoholic Steatohepatitis: The Possible Role of Physical Exercise

Passos, Emanuel; Ascensão, António; Martins, Maria João; Magalhães, José

doi:10.1016/j.metabol.2015.02.003

Cited by 35 publications

(41 citation statements)

References 126 publications

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“…It is well known that lipogenesis is the primary pathway by which ER stress induces hepatic steatosis. 7,8) To determine the mechanism involved in gomisin N-mediated improvement in hepatic steatosis, we measured the expression of the lipogenic genes such as fatty acid synthase (FAS), acetyl-coenzyme A carboxylase 1 (ACC1), and glycerol-3-phosphate acyltransferase (GPAT) in HepG2 cells treated with palmitate. As shown in Fig.…”

Section: Gomisin N Downregulates the Expression Of Inflammatory And Lmentioning

confidence: 99%

“…[2][3][4][5] ER stress contributes to development of insulin resistance and hepatic steatosis in non-alcoholic fatty liver disease (NAFLD). [6][7][8][9] NAFLD is a common hepatic disorder that is characterized by excessive lipid accumulation in the liver. The first stage consists of hepatic steatosis caused by triglyceride (TG) accumulation in hepatocytes.…”

mentioning

confidence: 99%

“…It has been reported that ER stress is an important pathological factor in this pathological process. [6][7][8][9] Thus, an agent that can attenuate ER stress may be a good therapeutic option for the treatment of NAFLD.…”

mentioning

confidence: 99%

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Protective Effect of Gomisin N against Endoplasmic Reticulum Stress-Induced Hepatic Steatosis

Jang

Yun

Kim

et al. 2016

Biological & Pharmaceutical Bulletin

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Gomisin N is a physiological substance derived from Schisandra chinensis. In the present study, the in vitro and in vivo effects of gomisin N on endoplasmic reticulum (ER) stress and hepatic steatosis were investigated. We quantified the expression of markers of ER stress, including glucose regulated protein 78 (GRP78), CCAAT/enhancer binding protein (C/EBP) homolog protein (CHOP), and X-box-binding protein-1 (XBP-1), and triglyceride (TG) accumulation, in HepG2 cells treated with tunicamycin or palmitate. Tunicamycin treatment in HepG2 cells induced expression of markers of ER stress and increased TG levels; Gomisin N reversed these effects, reducing the expression of markers of ER stress and TG levels. Similar effects were seen following palmitate pretreatment of HepG2 cells. The inhibitory effects of gomisin N were further confirmed in mice injected with tunicamycin. Gomisin N reduced expression of markers of ER stress and decreased TG levels in mouse liver after tunicamycin injection. Furthermore, gomisin N decreased expression of inflammatory and lipogenic genes in palmitate-incubated HepG2 cells. These results suggest that gomisin N inhibits ER stress and ameliorates hepatic steatosis induced by ER stress. Key words gomisin N; endoplasmic reticulum (ER) stress; hepatic steatosis; lipogenesis; inflammationThe endoplasmic reticulum (ER) plays critical roles in the synthesis of secreted and membrane proteins by mediating protein folding, production of lipids and sterols, and the storage of intracellular Ca 2+ . 1) However, pathological factors that disrupt ER homeostasis lead to the accumulation of unfolded protein in the ER lumen, provoking ER stress. Cells usually survive early stress by attenuating protein translation, removing unfolded proteins, and upregulating protein chaperons via the unfolded protein response (UPR).1) However, prolonged ER stress can lead to cell death and cause several diseases including ischemia/reperfusion injury, heart disease, and diabetes. [2][3][4][5] Recent studies show that hepatic ER stress is observed in metabolic diseases such as obesity and diabetes.2-5) ER stress contributes to development of insulin resistance and hepatic steatosis in non-alcoholic fatty liver disease (NAFLD). [6][7][8][9]

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Section: Gomisin N Downregulates the Expression Of Inflammatory And Lmentioning

confidence: 99%

mentioning

confidence: 99%

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Protective Effect of Gomisin N against Endoplasmic Reticulum Stress-Induced Hepatic Steatosis

Jang

Yun

Kim

et al. 2016

Biological & Pharmaceutical Bulletin

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“…Because the prevalence of NAFLD is increasing, it is necessary to develop agents that can prevent hepatic lipid accumulation and treat NAFLD-associated hepatic disorders. It has been reported that ER stress is an important pathological factor in this pathological process [2,17,20]. Thus, an agent that can attenuate ER stress may be a good therapeutic option for the treatment of NAFLD.…”

Section: Introductionmentioning

confidence: 99%

“…Recent studies show that hepatic ER stress is observed in metabolic diseases such as obesity and diabetes [1,3,23,26]. ER stress contributes to development of insulin resistance and hepatic steatosis in non-alcoholic fatty liver disease (NAFLD) [2,17,18,20]. NAFLD is a common hepatic disorder that is characterized by excessive lipid accumulation in the liver.…”

Section: Introductionmentioning

confidence: 99%

Gomisin A Ameliorates Endoplasmic Reticulum Stress-induced Hepatic Steatosis

Yun¹,

Jung²

2017

Journal of Life Science

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Previously, we have shown that Schisandra chinensis (Turcz.) Baill. (S. chinensis) has a protective effect against endoplasmic reticulum (ER) stress-induced hepatic steatosis. Gomisin A is a bioactive phytoestrogen derived from S. chinensis. In the present study, the in vitro and in vivo effects of gomisin A on ER stress and hepatic steatosis were investigated. We quantified the expression of markers of ER stress, including glucose regulated protein 78 (GRP78), C/EBP homolog protein (CHOP), and X-boxbinding protein-1 (XBP-1), in HepG2 cells treated with tunicamycin or palmitate. Tunicamycin treatment in HepG2 cells induced the expression of markers of ER stress, including GRP78, CHOP, and XBP-1c. However, treatment with gomisin A reduced the expression of markers of ER stress. These inhibitory effects were also observed in palmitate-incubated HepG2 cells. The in vivo inhibitory effects of gomisin A were assessed in mice injected with tunicamycin or fed with a high fat diet (HFD). Gomisin A reduced the expression of markers of ER stress and decreased triglyceride levels in the livers of mice after tunicamycin injection or HFD feeding. Furthermore, gomisin A decreased the expression of inflammatory genes in palmitate-incubated HepG2 cells and the liver of HFD-fed obese mice. These results suggest that gomisin A inhibits ER stress and ameliorates hepatic steatosis induced by ER stress.

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Scallop mantle toxin induces apoptosis in liver tissues of mice

Kariya

Hasegawa

2020

Food Science & Nutrition

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We had previously shown that the intake of scallop mantle tissue resulted in the death of mice and rats. In this study, we investigated the liver injury caused by mantle tissue to clarify the mechanism behind its toxicity. Mantle toxin increased lipid peroxidation and decreased the reductive thiol content as well as the DPPH radical scavenging activity, catalase activity, and glutathione content in the liver of the mice. These results suggested that the mantle tissue diet caused oxidative stress through the decrease in antioxidants. In addition, mantle toxin increased the mRNA expression of endoplasmic reticulum (ER) stress‐ and inflammation‐induced genes and the protein expression of caspase‐3 and Bax (which induce apoptosis), suggesting that the mantle tissue diet causes apoptosis through oxidative stress, ER stress, and inflammation in the liver tissue. Such liver injury may be an essential cause of the rodent demise.

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Endoplasmic Reticulum Stress Response in Non-alcoholic Steatohepatitis: The Possible Role of Physical Exercise

Cited by 35 publications

References 126 publications

Protective Effect of Gomisin N against Endoplasmic Reticulum Stress-Induced Hepatic Steatosis

Protective Effect of Gomisin N against Endoplasmic Reticulum Stress-Induced Hepatic Steatosis

Gomisin A Ameliorates Endoplasmic Reticulum Stress-induced Hepatic Steatosis

Scallop mantle toxin induces apoptosis in liver tissues of mice

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