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Upregulation of hepatic CD36 via glucocorticoid receptor activation contributes to dexamethasone-induced liver lipid metabolism disorder in mice
Toxicol Lett. 2022 May 16:S0378-4274(22)00091-1. doi: 10.1016/j.toxlet.2022.05.003. Online ahead of print.ABSTRACTGlucocorticoids such as dexamethasone (DEX) are widely prescribed to treat numerous conditions and diseases. However, glucocorticoid-induced liver lipid metabolism disorder, even nonalcoholic fatty liver disease, has caused extensive attention. Since fatty acid transporters such as CD36 and FATP play crucial roles in hepatic fatty acid uptake, this work examined their potential involvement in DEX-induced liver lipid accumulation. Chronic DEX administration (1-5mg/kg/day over 28 days) induced hepatic lipid accum...
Source: Toxicology Letters - May 19, 2022 Category: Toxicology Authors: Mingyang Chen Mengru Bai Yaodong Yi Shuanghui Lu Jun Luo Ping Li Hengbin Zhang Huidi Jiang Hui Zhou Source Type: research

Carnosol alleviates nonalcoholic fatty liver disease by inhibiting mitochondrial dysfunction and apoptosis through targeting of PRDX3
In conclusion, CAR suppressed lipid accumulation, mitochondrial dysfunction and hepatocyte apoptosis by activating PRDX3, mitigating the progression of NAFLD, and thus, CAR may represent a promising candidate for clinical treatment of steatosis.PMID:34678374 | DOI:10.1016/j.taap.2021.115758
Source: Toxicology and Applied Pharmacology - October 22, 2021 Category: Toxicology Authors: Yunfei Geng Yue Wang Ruimin Sun Xiaohui Kang Huanyu Zhao Meiyang Zhu Yu Sun Yan Hu Zhecheng Wang Xiaofeng Tian Yan Zhao Jihong Yao Source Type: research

Hesperetin protects against palmitate-induced cellular toxicity via induction of GRP78 in hepatocytes.
In conclusion, hesperetin protected against palmitate-induced hepatic cell death via activation of the sXBP1/GRP78 signaling pathway, thus inhibiting palmitate-induced ER stress. Moreover, high concentrations of hesperetin induce ER stress and subsequently cause cell death in hepatocytes. PMID: 32763355 [PubMed - as supplied by publisher]
Source: Toxicology and Applied Pharmacology - August 4, 2020 Category: Toxicology Authors: Geng Y, Wu Z, Buist-Homan M, Blokzijl H, Moshage H Tags: Toxicol Appl Pharmacol Source Type: research

Prenatal caffeine exposure increases the susceptibility to non-alcoholic fatty liver disease in female offspring rats via activation of GR-C/EBP α-SIRT1 pathway.
This study aimed to evaluate female adult offspring induced by prenatal caffeine exposure (PCE) are susceptible to non-alcoholic fatty liver disease (NAFLD) and to explore the underlying programming mechanisms. Pregnant rats were intragastrically administered caffeine (30, 60, and 120 mg/kg.d) on gestational day (GD) 9-20. The female adult offspring were randomly divided into three groups: offspring without or with chronic stress during postnatal week (PW) 10-12 and PW28 offspring. Results showed that PW28 PCE female offspring had a higher hepatic triglyceride content and Kleiner scores, accompanied by elevated serum cor...
Source: Toxicology - February 15, 2019 Category: Toxicology Authors: Hu S, Xia L, Luo H, Xu Y, Yu H, Xu D, Wang H Tags: Toxicology Source Type: research

Exendin-4, a glucagon-like peptide-1 receptor agonist, reduces hepatic steatosis and endoplasmic reticulum stress by inducing nuclear factor erythroid-derived 2-related factor 2 nuclear translocation.
Abstract Activation of endoplasmic reticulum (ER) stress is involved in the development of nonalcoholic fatty liver disease. Glucagon-like peptide-1 (GLP-1) has been reported to reduce hepatic steatosis, but the underlying mechanism has not been fully elucidated. Here, we investigated whether exendin-4 (EX-4), a GLP-1 receptor analogue, improves hepatic steatosis through ER stress reduction. Furthermore, we explored which ER stress pathway is involved in this process, with a focus on the protein kinase RNA-like ER kinase (PERK)-nuclear factor erythroid-derived 2-related factor 2 (Nrf2) pathway. EX-4 treatment redu...
Source: Toxicology and Applied Pharmacology - September 22, 2018 Category: Toxicology Authors: Yoo J, Cho IJ, Jeong IK, Ahn KJ, Chung HY, Hwang YC Tags: Toxicol Appl Pharmacol Source Type: research

Hepatocyte-protective effect of nectandrin B, a nutmeg lignan, against oxidative stress: Role of Nrf2 activation through ERK phosphorylation and AMPK-dependent inhibition of GSK-3 β.
This study investigated the hepatocyte-protective effect of nectandrin B against tert-butylhydroperoxide-induced oxidative injury and the underlying molecular mechanism. The cell viability assay revealed that nectandrin B prevents apoptosis stimulated by tert-butylhydroperoxide in both HepG2 cells and primary mouse hepatocytes. Nectandrin B also attenuated ROS production and restored the depleted glutathione level. Real-time PCR and immunoblot analyses showed that the expression of glutamate-cysteine ligase, an enzyme responsible for the glutathione biosynthesis, was induced by nectandrin B, indicating its indirect antioxi...
Source: Toxicology and Applied Pharmacology - August 6, 2016 Category: Toxicology Authors: Song JS, Kim EK, Choi YW, Oh WK, Kim YM Tags: Toxicol Appl Pharmacol Source Type: research

RNAi in murine hepatocytes: the agony of choice-a study of the influence of lipid-based transfection reagents on hepatocyte metabolism.
In conclusion, these findings demonstrate that the choice of non-viral siRNA delivery agent is critical in hepatocytes. This should be remembered, especially if RNA silencing is used for studying hepatic lipid homeostasis and its regulation. PMID: 26233687 [PubMed - as supplied by publisher]
Source: Archives of Toxicology - August 2, 2015 Category: Toxicology Authors: Böttger J, Arnold K, Thiel C, Rennert C, Aleithe S, Hofmann U, Vlaic S, Sales S, Shevchenko A, Matz-Soja M Tags: Arch Toxicol Source Type: research