Parası kalmadığı için otobüse binemiyordur ailesi porno izle ona daha yeni para gönderdiği için tekrar porno istemeye utanınca mecburen otostop çekmek için youporn çantasını alarak yol kenarına gelir etekli porno liseli türk kız yol kenarında dururken yanına yaklaşan porno kibar bir gencin onu gideceği yere kadar bırakmak porno izle istemesine çok mutlu olur arabaya bindiklerinde gideceği yer ile porno arabayı kullanan adamın gittiği yer arasında çok mesafe sex izle farkı olduğunu anlayan türk kız bu yaptığı porno indir iyilik karşısında arabada ona memelerini açar porno sapıklaşan adam yol kenarındaki hotelde durarak porno izle üniversiteli otostop çeken türk kızına odada sakso çektirip sikerExpression of Endoplasmic Reticulum Stress-Associated Protein IRE1 and JNK in Lung Tissues of Smoking Induced COPD Model Rats| Abstract

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Abstract

Expression of Endoplasmic Reticulum Stress-Associated Protein IRE1 and JNK in Lung Tissues of Smoking Induced COPD Model Rats

Author(s): Li-Le Wang, Rui-Cheng Hu*, Shuang-Xiang Tan, Ai-Guo Dai, Jian-Lu Su, Ming Xu, Chun-Chu Kong, Yun-Rong Chen, Dai-Yan Fu, Jie Li, Gui-Xiang Gan, Chang-Yu Huang, Bin-Bin Chen and Mo Liang (China)

Aim: To investigate the expression of IRE1 (inositol-requiringenzyme 1) and JNK (c-Jun N-terminal kinase) in lung tissue of cigarette smoke (CS) induced chronic obstructive pulmonary disease (COPD) rats.

Methods: Adult male Wistar rats (n=40) were randomly divided into 4 groups with 10 rats in each group: control group, CS-2 group (exposed to CS for 2 months), CS-4 group (exposed to CS for 4 months) and ex-smoking group (quit smoking for 1 month after exposed to CS for 4 months). The percentage of forced expiratory volume in 0.3 seconds to forced vital capacity (FEV0.3/FVC) and peak expiratory flow (PEF) were measured. TUNEL assay was used to detect apoptotic cells. Immunohistochemistry and Western blotting were used to detect the expression of IRE1, P-IRE1, JNK and P-JNK proteins.

Results: The pulmonary of function greatly decreased in the rats exposed to CS for 2 months in comparison with control group (P<0.05), markedly decreased in the rats exposed to CS for 4 months as compared with the rats after exposure to CS for 2 months (P<0.05) and was improved little in ex-smoking rats (P>0.05). The apoptotic cells were markedly increased in the rats exposed to CS for 2 months and were ever more in the rats exposed to CS for 4 months. The apoptotic cells were alveolar epithelial cell â… (ACEâ… ), ACE â…¡, vascular endothelial cells and bronchial epithelial cells. The protein level of p-IRE1 (phospho-inositol-requiringenzyme 1) and p-JNK (phospho-c-Jun N-terminal kinase) were remarkably increased in the rats after exposure to CS for 2 months compared with the control rats (P<0.05), significantly elevated in the rats exposed to CS for 4 months (P>0.05).

Conclusion: CS promotes the development of COPD by inducing the expression of endoplasmic reticulum stress-associated protein IRE1 and JNK.  


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