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The expression of autophagy-related protein in the model of fat embolism syndrome in rats |
Zhang Ying, Xu Xiao-tao, Wang Ai-zhong |
Department of Anesthesiology, Shanghai Sixth People′s Hospital East Affiliated to Shanghai University of Medicine & Health Sciences, Shanghai 201306, China |
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Abstract Objective To observe the expression of autophagy-related protein in the model of fat embolism syndrome in rats. Methods Sixty healthy male SD rats, weighing (250±20) g, were assigned to control group (FES 0 h group), FES 1 h group, FES 6 h group, FES 12 h group and FES 24 hgroup, according to the random number table. Allogeneic perinephric fat (0.706 mL/kg) was injected through rat caudal veins in FES group. Instead isotonic saline in an equal volume was given to rats in control group. The rats in the fat embolism + Rapamycin group received the autophagy activator Rapamycin by intraperitoneal injection at a dosage of 2 mg/kg 30 minutes before fat injection. Lung samples were harvested from each group to detect pathological morphology, lung weight to dry ratio (W/D), and activity in myeloperoxidase (MPO) was detected by real-time reverse transcriptase polymerase chain reaction (RT-PCR). The protein expression of autophagy was detected by Western blot. Results Compared with control group, lung tissues in FES group were seriously injured. Lung W/D value and activity of MPO in lung tissue were higher in FES group than those in control group (P<0.05). Compared with control group, the expression of p62, mTOR/p- mTOR and p70S6K/p- p70S6K protein was up-regulated in FES group (P<0.05). The expression of p62, mTOR/p-mTOR and p70S6K/p- p70S6K protein was down-regulated in the FES 24 h+Rapamycin group compared to the FES 24 h group (P<0.05). Conclusion Autophagy is involved in the pathogenesis of FES, and it is inhibited in the model of fat embolism syndrome.
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Corresponding Authors:
Wang Ai-zhong, E-mail: w19680420@sohu.com
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