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Effect of mild hypothermia preconditioning against low temperature (4°C) induced rat liver cell injury in vitro.

ABSTRACT: Bioartificial liver holds special position in the field of regenerative medicine, and cold environment at 4? is widely used for the short storage of both organ and liver cell for later application. However, the disadvantages of such cold storage could influence cell viability and lead to cell apoptosis in different degrees. In this study, we mainly explore the pre-protective effect of mild hypothermia against low temperature (4?)-induced rat liver cell injury in vitro. Our results indicated that the precondition with mild hypothermia could increase cell viability, such as cell proliferation, LDH regulation and glycogen synthesis ability of liver cell. The precondition also decreased the ROS production and relieved cell apoptosis in liver cells. Compared with the model group, the mitochondrial membrane potential was restored in the mild hypothermia group, as well as the mitochondrial membrane permeability transition pore opening, indicating that the therapeutic mechanism was related to mitochondrial protection. Further analysis showed that PI3K-Akt-GSK3? signal pathway might be associated with the pre-protective effect of mild hypothermia. Thus, our study suggested that the precondition with mild hypothermia hold the protective effect for liver cell in cold environment, and further developed a novel strategy for the storage of liver seed cells, even bioartificial liver.

SUBMITTER: Qin J

PROVIDER: S-EPMC5409157 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Effect of mild hypothermia preconditioning against low temperature (4°C) induced rat liver cell injury in vitro.

Qin Jiasheng J Mai Yanxing Y Li Yang Y Jiang Zesheng Z Gao Yi Y

PloS one 20170428 4

Bioartificial liver holds special position in the field of regenerative medicine, and cold environment at 4℃ is widely used for the short storage of both organ and liver cell for later application. However, the disadvantages of such cold storage could influence cell viability and lead to cell apoptosis in different degrees. In this study, we mainly explore the pre-protective effect of mild hypothermia against low temperature (4℃)-induced rat liver cell injury in vitro. Our results indicated that ...[more]

PMID: 28453529

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Project description:IntroductionCholestasis is characterized by accumulation of bile acids and inflammation, causing hepatocellular damage. Still, liver damage markers are highest in acute cholestasis and drop when this condition becomes chronic, indicating that hepatocytes adapt towards the hostile environment. This may be explained by a hormetic response in hepatocytes that limits cell death during cholestasis.AimTo investigate the mechanisms that underlie the hormetic response that protect hepatocytes against experimental cholestatic conditions.MethodsHepG2.rNtcp cells were preconditioned (24 h) with sub-apoptotic concentrations (0.1-50 ?M) of various bile acids, the superoxide donor menadione, TNF-? or the Farsenoid X Receptor agonist GW4064, followed by a challenge with the apoptosis-inducing bile acid glycochenodeoxycholic acid (GCDCA; 200 ?M for 4 h), menadione (50 ?M, 6 h) or cytokine mixture (CM; 6 h). Levels of apoptotic and necrotic cell death, mRNA expression of the bile salt export pump (ABCB11) and bile acid sensors, as well as intracellular GCDCA levels were analyzed.ResultsPreconditioning with the pro-apoptotic bile acids GCDCA, taurocholic acid, or the protective bile acids (tauro)ursodeoxycholic acid reduced GCDCA-induced caspase-3/7 activity in HepG2.rNtcp cells. Bile acid preconditioning did not induce significant levels of necrosis in GCDCA-challenged HepG2.rNtcp cells. In contrast, preconditioning with cholic acid, menadione or TNF-? potentiated GCDCA-induced apoptosis. GCDCA preconditioning specifically reduced GCDCA-induced cell death and not CM- or menadione-induced apoptosis. The hormetic effect of GCDCA preconditioning was concentration- and time-dependent. GCDCA-, CDCA- and GW4064- preconditioning enhanced ABCB11 mRNA levels, but in contrast to the bile acids, GW4064 did not significantly reduce GCDCA-induced caspase-3/7 activity. The GCDCA challenge strongly increased intracellular levels of this bile acid, which was not lowered by GCDCA-preconditioning.ConclusionsSub-toxic concentrations of bile acids in the range that occur under normal physiological conditions protect HepG2.rNtcp cells against GCDCA-induced apoptosis, which is independent of FXR-controlled changes in bile acid transport.

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Effect of mild hypothermia preconditioning against low temperature (4°C) induced rat liver cell injury in vitro.

Publications

Effect of mild hypothermia preconditioning against low temperature (4°C) induced rat liver cell injury in vitro.

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