The mechanism of endoplasmic reticulum stress in the acute liver injury in mice
LI Yong-hua
TAO Li
LIN Yin
LI Guang-yu
CHEN Chang
Abstract:Objective To investigate the change and mechanism of endoplasmic reticulum (ER) stress in acute liver injury induced by carbon tetrachloride (CCl4 ) in mice.Methods Thirty C57BL/6 mice were randomly allocated to treatment group and control group (n =15).Treatment group was given CCl 4 (20%/0.1 mL/10 g) intraperitoneally to es-tablish acute liver injury models, and olive oil was given as placebo in the control group .The expressions of ER stress -related proteins and apoptotic proteins in the liver were determined by pathological staining .The trends of ER stress -re-lated proteins and apoptotic proteins were also analyzed by Western blot .Results According to pathological analysis , that administration of CCl4 caused marked hepatic injury , characterized by significant expressions of ER stress -related pro-teins and apoptotic proteins combined with a remarkable reduction of proliferative proteins PCNA .TUNEL staining and PCNA staining showed that significant increasing apoptotic cells and reduced proliferative cells , respectively, when com-pared with the control group (P <0.05).By the same time, Western blot analysis also demonstrated that administration of CCl4 to mice caused significant elevated expression of ER stress -related proteins and apoptotic proteins , accompanied with the release of mitochondrial cytochrome c and obvious repression of proliferative proteins , such as p -Akt and PCNA. Conclusion ER stress -mediated mitochondrial apoptotic pathway plays an important role in the pathogenesis of CCl 4 -induced acute liver injury in mice.
Keywords:endoplasmic reticulum stressacute liver injuryapoptosiscarbon tetrachloride
Publication Date:2015-01-01
Online Publishing Date:2025-08-15(First online date of this platform, not the publication date of the document)
Pages:4( 35-38 )
Guangdong Medical Journal

Guangdong Medical Journal

PKUISTIC
ISSN:1001-9448
Year, Vol.(Issue):2015,(1)