Artemisia iwayomogiplusCurcuma longaSynergistically Ameliorates Nonalcoholic Steatohepatitis in HepG2 Cells

The combination ofArtemisia iwayomogiandCurcuma longaradix is frequently prescribed for liver diseases in TKM. However, the synergic effects of the two herbs on nonalcoholic steatohepatitis (NASH) have not yet been studied. Therefore, we investigated the anti-NASH effects of the water extract ofA. iwayomogi(AI),C. longaradix (CL), and combination of the two herbs (ACE). Hepatic steatosis and NASH were induced in HepG2 cells by treatment with palmitic acid (PA, for 6 h) with/without pretreatment of ACE (25 or 50 μg/mL), AI (50 or 100 μg/mL), CL (50 or 100 μg/mL), curcumin (5 μg/mL), or scopoletin (5 μg/mL). The PA treatment (200 μM) drastically altered intracellular triglyceride levels, total cholesterol, and expression levels of genes related to lipid metabolism (CD36, SREBP1c, PPAR-γ, and PPAR-α), whereas pretreatment with ACE significantly attenuated these alterations. ACE also protected HepG2 cells from PA- (300 μM-) induced endoplasmic reticulum (ER) stress and apoptosis and attenuated the related key molecules including GRP78, eIF2, and CHOP, respectively. In conclusion, we found synergic effects ofA. iwayomogiandC. longaon NASH, supporting the clinical potential for fatty liver disorders. In addition, modulation of ER stress-relative molecules would be involved in its underlying mechanism.

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Rosmarinic acid attenuates hepatic steatosis by modulating ER stress and autophagy in oleic acid-induced HepG2 cells

RSC Advances ◽

10.1039/c8ra02849d ◽

2018 ◽

Vol 8 (47) ◽

pp. 26656-26663 ◽

Cited By ~ 4

Author(s):

Govindaraj Jayanthy Balachander ◽

Sorimuthupillai Subramanian ◽

Kaliappan Ilango

Keyword(s):

Oleic Acid ◽

Fatty Acid ◽

Er Stress ◽

Hepatic Steatosis ◽

Rosmarinic Acid ◽

Hepg2 Cells ◽

Liver Disorders

Non-alcoholic fatty acid disease (NAFLD) has become an emerging entity of liver disorders worldwide.

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Effects of Ulmus macrocarpa Hance Water Extract on Lipid Metabolism in HepG2 Cells

Journal of the Korean Society of Food Science and Nutrition ◽

10.3746/jkfn.2019.48.11.1186 ◽

2019 ◽

Vol 48 (11) ◽

pp. 1186-1194

Author(s):

Tae Hee Kim ◽

Jeong Jun Lee ◽

Jungkee Kwon ◽

Chang Hoon Lee

Keyword(s):

Lipid Metabolism ◽

Hepg2 Cells ◽

Water Extract

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Aqueous Extract of Pepino Leaves Ameliorates Palmitic Acid-Induced Hepatocellular Lipotoxicity via Inhibition of Endoplasmic Reticulum Stress and Apoptosis

Antioxidants ◽

10.3390/antiox10060903 ◽

2021 ◽

Vol 10 (6) ◽

pp. 903

Author(s):

Jen-Ying Hsu ◽

Hui-Hsuan Lin ◽

Charng-Cherng Chyau ◽

Zhi-Hong Wang ◽

Jing-Hsien Chen

Keyword(s):

Fatty Acid ◽

Palmitic Acid ◽

Er Stress ◽

Lipid Accumulation ◽

Hepg2 Cells ◽

Target Genes ◽

Liver Lipid ◽

Antioxidant Response ◽

Long Chain Fatty Acid ◽

Nrf2 Expression

Saturated fatty acid is one of the important nutrients, but contributes to lipotoxicity in the liver, causing hepatic steatosis. Aqueous pepino leaf extract (AEPL) in the previous study revealed alleviated liver lipid accumulation in metabolic syndrome mice. The study aimed to investigate the mechanism of AEPL on saturated long-chain fatty acid-induced lipotoxicity in HepG2 cells. Moreover, the phytochemical composition of AEPL was identified in the present study. HepG2 cells treated with palmitic acid (PA) were used for exploring the effect of AEPL on lipid accumulation, apoptosis, ER stress, and antioxidant response. The chemical composition of AEPL was analyzed by HPLC-ESI-MS/MS. AEPL treatment reduced PA-induced ROS production and lipid accumulation. Further molecular results revealed that AEPL restored cytochrome c in mitochondria and decreased caspase 3 activity to cease apoptosis. In addition, AEPL in PA-stressed HepG2 cells significantly reduced the ER stress and suppressed SREBP-1 activation for decreasing lipogenesis. For defending PA-induced oxidative stress, AEPL promoted Nrf2 expression and its target genes, SOD1 and GPX3, expressions. The present study suggested that AEPL protected from PA-induced lipotoxicity through reducing ER stress, increasing antioxidant ability, and inhibiting apoptosis. The efficacy of AEPL on lipotoxicity was probably concerned with kaempferol and isorhamnetin derived compounds.

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A hot water extract of turmeric (Curcuma longa) suppresses acute ethanol-induced liver injury in mice by inhibiting hepatic oxidative stress and inflammatory cytokine production

Journal of Nutritional Science ◽

10.1017/jns.2016.43 ◽

2017 ◽

Vol 6 ◽

Cited By ~ 16

Author(s):

Ryusei Uchio ◽

Yohei Higashi ◽

Yusuke Kohama ◽

Kengo Kawasaki ◽

Takashi Hirao ◽

...

Keyword(s):

Oxidative Stress ◽

Liver Injury ◽

Oral Administration ◽

Alanine Aminotransferase ◽

Curcuma Longa ◽

Water Extract ◽

Hot Water ◽

Hepatic Tissue ◽

Hot Water Extract ◽

Acute Ethanol

AbstractTurmeric (Curcuma longa) is a widely used spice that has various biological effects, and aqueous extracts of turmeric exhibit potent antioxidant activity and anti-inflammatory activity. Bisacurone, a component of turmeric extract, is known to have similar effects. Oxidative stress and inflammatory cytokines play an important role in ethanol-induced liver injury. This study was performed to evaluate the influence of a hot water extract of C. longa (WEC) or bisacurone on acute ethanol-induced liver injury. C57BL/6 mice were orally administered WEC (20 mg/kg body weight; BW) or bisacurone (60 µg/kg BW) at 30 min before a single dose of ethanol was given by oral administration (3·0 g/kg BW). Plasma levels of aspartate aminotransferase and alanine aminotransferase were markedly increased in ethanol-treated mice, while the increase of these enzymes was significantly suppressed by prior administration of WEC. The increase of alanine aminotransferase was also significantly suppressed by pretreatment with bisacurone. Compared with control mice, animals given WEC had higher hepatic tissue levels of superoxide dismutase and glutathione, as well as lower hepatic tissue levels of thiobarbituric acid-reactive substances, TNF-α protein and IL-6 mRNA. These results suggest that oral administration of WEC may have a protective effect against ethanol-induced liver injury by suppressing hepatic oxidation and inflammation, at least partly through the effects of bisacurone.

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Effect of a water extract of Curcuma longa on emotional states in healthy participants

Bioscience of Microbiota Food and Health ◽

10.12938/bmfh.17-020 ◽

2018 ◽

Vol 37 (2) ◽

pp. 25-29 ◽

Cited By ~ 3

Author(s):

Kengo KAWASAKI ◽

Koutarou MUROYAMA ◽

Shinji MUROSAKI

Keyword(s):

Curcuma Longa ◽

Water Extract ◽

Emotional States ◽

Healthy Participants

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Micronized Palmitoylethanolamide Ameliorates Methionine- and Choline-Deficient Diet–Induced Nonalcoholic Steatohepatitis via Inhibiting Inflammation and Restoring Autophagy

Frontiers in Pharmacology ◽

10.3389/fphar.2021.744483 ◽

2021 ◽

Vol 12 ◽

Author(s):

Jiaji Hu ◽

Hanglu Ying ◽

Jie Yao ◽

Longhe Yang ◽

Wenhui Jin ◽

...

Keyword(s):

Nonalcoholic Steatohepatitis ◽

Underlying Mechanism ◽

Protective Role ◽

Hepatocellular Injury ◽

Deficient Diet ◽

Neuroprotective Effects ◽

Pathway Activation ◽

Elevated Expression ◽

Anti Inflammatory

Nonalcoholic steatohepatitis (NASH) has become one of the serious causes of chronic liver diseases, characterized by hepatic steatosis, hepatocellular injury, inflammation and fibrosis, and lack of efficient therapeutic agents. Palmitoylethanolamide (PEA) is an endogenous bioactive lipid with various pharmacological activities, including anti-inflammatory, analgesic, and neuroprotective effects. However, the effect of PEA on nonalcoholic steatohepatitis is still unknown. Our study aims to explore the potential protective role of PEA on NASH and to reveal the underlying mechanism. In this study, the C57BL/6 mice were used to establish the NASH model through methionine- and choline-deficient (MCD) diet feeding. Here, we found that PEA treatment significantly improved liver function, alleviated hepatic pathological changes, and attenuated the lipid accumulation and hepatic fibrosis in NASH mice induced by MCD diet feeding. Mechanistically, the anti-steatosis effect of PEA may be due to the suppressed expression of ACC1 and CD36, elevated expression of PPAR-α, and the phosphorylation levels of AMPK. In addition, hepatic oxidative stress was greatly inhibited in MCD-fed mice treated with PEA via enhancing the expression and activities of antioxidant enzymes, including GSH-px and SOD. Moreover, PEA exerted a clear anti-inflammatory effect though ameliorating the expression of inflammatory mediators and suppressing the NLRP3 inflammasome pathway activation. Furthermore, the impaired autophagy in MCD-induced mice was reactivated with PEA treatment. Taken together, our research suggested that PEA protects against NASH through the inhibition of inflammation and restoration of autophagy. Thus, PEA may represent an efficient therapeutic agent to treat NASH.

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Effect of Cold Water Extract from Luffa cylindrical on Intracellular Triglyceride and Free Glycerol Release Level in Lipolysis of Differentiated 3T3‐L1 Adipocytes

The FASEB Journal ◽

10.1096/fasebj.24.1_supplement.lb256 ◽

2010 ◽

Vol 24 (S1) ◽

Author(s):

Jiwon Yang ◽

Ja‐Young Jang ◽

Ok‐Kyung Kim ◽

Jeongmin Lee ◽

...

Keyword(s):

Cold Water ◽

Water Extract ◽

Free Glycerol ◽

Glycerol Release ◽

Intracellular Triglyceride

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Combination of isoflurane and propofol, a means for general anesthesia in the orthopedic surgery of perioperative cerebral hypoperfusion rats to avoid cognitive impairment Anesthesia of perioperative cerebral hypoperfusion

10.21203/rs.2.14325/v4 ◽

2020 ◽

Author(s):

Xinyue Bu ◽

Tang Li ◽

Haiyun Wang ◽

Zhengyuan Xia ◽

Di Guo ◽

...

Keyword(s):

Cognitive Impairment ◽

Cognitive Function ◽

Er Stress ◽

General Anesthesia ◽

Underlying Mechanism ◽

Cerebral Hypoperfusion ◽

Nissl Staining ◽

Aging Rats ◽

Biochemical Analyses ◽

Common Carotid Arteries

Abstract Background: Perioperative cerebral hypoperfusion often occurs. However, the underlying mechanism of cognitive impairment resulting when perioperative cerebral hypoperfusion occurs remain mostly to be determined. Anesthetic isoflurane induces neuronal injury via endoplasmic reticulum (ER) stress, whereas sub-anesthetic dose of propofol improves postoperative cognitive function. However, the effects of the combination of isoflurane plus propofol, which is a common combination of anesthesia for patient, on ER stress and the associated cognitive function remain unknown. Methods: We therefore set out to determine the effects of isoflurane plus propofol on the ER stress and cognitive function in the rats insulted by cerebral hypoperfusion. A ligation of bilateral common carotid arteries (CCA) surgery was adopted to prepare rats as cerebral hypoperfusion (CH) animal model. A second surgery, open reduction and internal fixation (ORIF), requiring general anesthesia, was operated 30 days later so that the effects of anesthetics on cognitive function of these CH rats could be assessed. The rats received isoflurane alone (1.9%), propofol alone (40 mg·kg -1 ·h -1 ) or a combination of isoflurane and propofol (1% and 20 mg·kg -1 ·h -1 or 1.4% and 10 mg·kg -1 ·h -1 ). Behavior studies (Fear Conditioning test), histological analyses (Nissl staining) and biochemical analyses (western blotting for the harvested rat brain tissues) were employed in the studies. Results: We found that the combination of 1% isoflurane plus 20 mg·kg -1 ·h -1 propol did not aggravate the cognitive impairment and the ER stress in aging rats with cerebral hypoperusion and being subjected to an ORIF surgery. Conclusions: These data suggest that ER stress contributes to the underlying mechanism of cognitive impairment and the combination of isoflurane and propofol did not aggravate the cognitive impairment and the ER stress in aging rats with cerebral hypoperfusion and being subjected to an ORIF surgery.

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Selective Activation of Endoplasmic Reticulum Stress by Reactive-Oxygen-Species-Mediated Ochratoxin A-Induced Apoptosis in Tubular Epithelial Cells

International Journal of Molecular Sciences ◽

10.3390/ijms222010951 ◽

2021 ◽

Vol 22 (20) ◽

pp. 10951

Author(s):

Chong-Sun Khoi ◽

Yu-Wen Lin ◽

Jia-Huang Chen ◽

Biing-Hui Liu ◽

Tzu-Yu Lin ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Endoplasmic Reticulum ◽

Er Stress ◽

Ochratoxin A ◽

Reactive Oxygen ◽

Underlying Mechanism ◽

Oxygen Species ◽

Food And Feed ◽

Renal Proximal Tubular Cells ◽

Induced Apoptosis

Ochratoxin A (OTA), one of the major food-borne mycotoxins, impacts the health of humans and livestock by contaminating food and feed. However, the underlying mechanism of OTA nephrotoxicity remains unknown. This study demonstrated that OTA induced apoptosis through selective endoplasmic reticulum (ER) stress activation in human renal proximal tubular cells (HK-2). OTA increased ER-stress-related JNK and precursor caspase-4 cleavage apoptotic pathways. Further study revealed that OTA increased reactive oxygen species (ROS) levels, and N-acetyl cysteine (NAC) could reduce OTA-induced JNK-related apoptosis and ROS levels in HK-2 cells. Our results demonstrate that OTA induced ER stress-related apoptosis through an ROS-mediated pathway. This study provides new evidence to clarify the mechanism of OTA-induced nephrotoxicity.

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