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The mechanism of endoplasmic reticulum stress in the acute liver injury in mice

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 CCl4( 20% /0. 1 m L/10 g) intraperitoneally to establish 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- related 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 proteins 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 compared 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 CCl4-induced acute liver injury in mice.