ObjectiveTo study the clinical effect of the combination of glucosamine hydrochloride with exercise therapy and traditional Chinese medicine hot compress in the treatment of early patellofemoral osteoarthritis. MethodsA total of 126 patients with early patellofemoral osteoarthritis treated between June 2013 and April 2015 were divided into group A (n=43), B (n=42) and C (n=41) with the method of random number table. Oral administration of glucosamine hydrochloride tablets, exercise therapy of knee joints and traditional Chinese medicine hot compress were applied for the 43 patients in group A. Oral administration of glucosamine hydrochloride tablets and exercise therapy of knee joints were applied for the 42 patients in group B. Exercise therapy of knee joints and traditional Chinese medicine hot compress were applied for the 41 patients in group C. Chen's Scoring was applied before the treatment and 2, 4, 12 and 24 weeks after the treatment. ResultsThe differences of Chen's scores at the time points after treatment and those before treatment of the same group had statistical significance (P<0.05). The differences of Chen's scores at the time points after treatment in group A and those in group B and C had statistical significance (P<0.05). There were no obvious adverse effects due to administration of glucosamine hydrochloride tablets in group A and B. Five patients in group A and 4 patients in group C suffered from the symptoms of local erythema, light cutaneous pruritus and other contact dermatitis after traditional Chinese medicine hot compress. Those symptoms disappeared automatically several hours later without any special treatment. ConclusionThe treatment of early patellofemoral osteoarthritis by the combination of glucosamine hydrochloride tablets with exercise therapy and traditional Chinese medicine hot compress can rapidly relieve joint pain, and maintain efficacy for a long time.
ObjectiveTo investigate the changes of autophage-related protein in lung tissues of rats with chronic obstructive pulmonary disease (COPD). MethodsPassive cigarette smoking was used to establish COPD model in rats. The mRNA and protein expressions of PI3K, total AKT, phosphorylated-AKT, total mTOR, phosphorylated-mTOR, and autophagy-related genes including LC3Ⅱ/Ⅰ, Beclin1, Atg5, Atg7, Atg12, P62 in lung tissues were measured by real-time PCR and Western blot. The autophagy level was compared between the COPD rats and the normal rats by LC3B immunohistochemistry. ResultsReal-time PCR analysis showed that the mRNA expressions of Beclin1, Atg5 and Atg12 significantly increased in lung tissues of the COPD rats compared with the normal rats (all P < 05). There was no significant difference between the COPD rats and the normal rats as for Atg7 mRNA expression (P > 0.05). Western blot analysis showed that the protein expressions of PI3K, p-AKT/AKT and p-mTOR/mTOR significantly decreased, the protein expressions of LC3 Ⅱ/Ⅰ, Atg5, and Beclin1 increased, and protein expression of P62 significantly decreased in lung tissues of the COPD rats compared with the normal rats (all P < 05). LC3B immunohistochemistry showed that the LC3B expression was higher in the COPD rats than that in the normal rats. ConclusionThe level of autophagy significantly increases in COPD rats with decreased expression of upstream proteins in autophagy signal pathway and increased expression of autophage proteins.
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.