ObjectiveTo investigate the role of PI3K/AKT/mTOR signaling pathway in skeletal muscle atrophy in rats with chronic obstructive pulmonary diseases(COPD). MethodsPassive cigarette smoking was used to establish COPD model.The protein expression of PI3K, total mTOR, phosphorylated-mTOR, total GSK-3β, phosphorylated-GSK-3β, total 4E-BP1, phosphorylated-4E-BP1, total p70S6K1 and phosphorylated-p70S6K1 in extensor digitorum longus of rats were measured by Western blot. ResultsThe protein expression of PI3K was not significantly different between two groups(P > 0.05).Compared with the control group, the protein expression of total mTOR, phosphorylated-mTOR, total GSK-3β, and phosphorylated-GSK-3βincreased significantly in the COPD group(P < 0.05).The protein expression of total 4E-BP1 and total p70S6K1 were not significantly different between two groups(P > 0.05).While the protein expression of phosphorylated-4E-BP1 and phosphorylated-p70S6K1 significantly increased in the COPD group(P < 0.05). ConclusionThe protein expressions of PI3K/AKT/mTOR signaling pathway in extensor digitorum longus increased significantly in COPD rats, suggesting that the activity of PI3K/AKT/mTOR signaling pathway increased, which may be one of the compensatory mechanism of skeletal muscle atrophy in COPD.
ObjectiveTo investigate the role of autophagy-lysosomal system in skeletal muscle atrophy in rats with chronic obstructive pulmonary disease (COPD). MethodsPassive cigarette smoking was used to establish COPD model. The mRNA and protein expression of FOXO transcription factor and autophagy-related genes Bnip3, Beclin1, p62, MAP-LC3Ⅱ/Ⅰ, Atg5 in extensor digitorum longus of rats were measured by real time PCR and Western blot. The changes of extensor digitorum longus tissue sections and lung tissue sections in the experimental group rats were observed under transmission electron microscopy. ResultsCompared with the control group, the mRNA expression of FOXO transcription factor and autophagy-related genes Bnip3, Beclin1, p62, Atg5 in extensor digitorum longus of the experimental group group rats was significantly increased (all P<0.05, as for Bnip3, the P value between two groups <0.01); The mRNA expression of MAP-LC3Ⅱ/Ⅰwas not significantly different between two groups (P>0.05). The protein expression of FOXO, Bnip3, Beclin1, p62, MAP-LC3Ⅱ/Ⅰ, Atg5 significantly increased in the COPD group (all P<0.05, as for Bnip3, MAP-LC3Ⅱ/Ⅰ, Beclin1, the P values between two groups <0.01). Compared with the control group, autolysosome in extensor digitorum longus tissue sections of the experimental group rats increased and lung tissue fibrosis and more inflammatory cells were observed in lung tissue sections of the experimental group rats under transmission electron microscopy. ConclusionThe mRNA and protein expressions of FOXO transcription factor and autophagy-related genes in extensor digitorum longus increase significantly in the experimental group rats, suggesting that the activity of autophagy-lysosomal system, which may be one mechanism of skeletal muscle atrophy in COPD.
Objective To improve the knowledge of pulmonary mucosa-associated lymphoid tissue (MALT)lymphoma. Methods A patient diagnosed as pulmonary MALT lymphoma was reported and related literatures were reviewed. Results The patient was a 58-year-old male,admitted due to intermittent fever,cough,sputum production,chest tightness and fatigue for 4 years.The patient was diagnosed as "pulmonary tuberculosis and tuberculous pleurisy" in other hospital and received anti-tuberculosis treatment for 3 years.The CT of the chest showed consolidation in the right middle lobe,right low lobe and left lower lobe with bronchial ventilation levy,miliary nodules in the right middle lobe,interstitial thickening,and right pleural effusion.Ultrasound guided lung biopsy pathology of the right lung showed diffuse small lymphocytes infiltration.The immunohistochemistry showed positive staining of CD20,CD79α and Vim,and weakly positive staining of Ki67(15%).Therefore,the patient was finally diagnosed pulmonary MALT lymphoma. Conclusions Pulmonary MALT lymphoma has no specific clinical manifestations,so is easy to be misdiagnosed as pulmonary tuberculosis,pneumonia or lung cancer.The patients with suspicious pulmonary MALT lymphoma should undergo percutaneous lung biopsy,transbronchial lung biopsy or open lung biopsy as soon as possible for immunohistochemistry staining to confirm the diagnosis.