The Mechanisms Of Mitochondria And Endoplasmic Reticulum Stress In Pressure Ulcers

Objectives To discuss mitochondria and endoplasmic ticulum stress of the mechanism in the pressure ulcer of the rats and its mediated apoptosis,studying the pathology mechanism of pressure ulcer deeply.To povide effective treatment for laboratory targets and basis theory for clinical treatment in the pressure ulcers.Methods According to the domestic li-ping jiang's Study of pressure ulcer model in rats model of pressure ulcers.According to random number table method, 40 Wistar rats is divided into the control group,3C group,6C group,9C group,12 C group on average.And at the end of the experiment,kill the rats and teke the issue of muscle.Making the HE?transmission electron micrlscopy(TEM) ? western blot and immunohistochemistry,to detect the change of the issure.The western blot detect GRP78?caspase-12?Bax?Bcl-2and immunohistochemistry detect GRP78 ? caspase-12 ? Bcl-2.Statistical analysis of data use SPSSl7.0 system,measurement date use(),differences between groups use one-way ANOVA with P<0.05 for statistical significance.sx ?Results HE shows that compared with the compression of the control group,the morphology of the muscle fibers is complete and neat.As the extension of cycle,the degradation of changes in muscle fiberss,for example,the structure of muscle fibers are disordered and appears dissolution and vacuolar degeneration,etc.The results of TEM are vertify the conculsion above,and aslo shows mitochondria's changes,for example,mitochonria's crest disappears and mitochonria occurs edema, vacuolar degeneration.Western blot shows that compared with the compression of the control group,others has elevated distinctly in GRP78 and the 6c,9c,12 c of Caspase-12,and difference was statistically significant.Then,the results of Bcl-2/Bax reflecting cell apoptosis shows that compared with the compression of the control group,the 3c group becomes slightly higher but has no statistical significance and the 6c,9c,12 c group becomes a significant decrease statistically.Conclusions 1 the pressure ulcers in rats activates ERS and its mediated apoptosis;2the pressure ulcers in rats caused the damage of mitochondria and its mediated apoptosis.