The Expression Of M-Calpain In Rat Skeletal Muscle In The Model Of Chronic Obstructive Pulmonary Disease | Posted on:2015-06-20 | Degree:Master | Type:Thesis | Country:China | Candidate:Q W Li | Full Text:PDF | GTID:2284330431492999 | Subject:Internal medicine | Abstract/Summary: | PDF Full Text Request | ObjectiveM-Calpain can degradate the cytoskeletal protein and participate in theapoptosis. The aim of this study was to study the expression and significance ofm-Calpain in COPD rat skeletal muscle atrophy.Methods40of healthy male Wistar rats aged10-12week old and weighted(220+32)g (fromExperimental Animal Center of the Zhengzhou University) were randomly divided into modelgroup (n=20) and control group (n=20), the COPD model was made by tabocco smoke inhalationand intracheally given LPS successfully while the control group rats were tested via exposure tonormal saline.5rats from each group were picked out for lung function tests at the28thday,subsequently was euthanized for the observation of the pathological changes in lung tissue andskeletal muscle at the29thday. Diaphragmatic muscle cell apoptosis rate was evaluated byTUNEL method; The expression of m-Calpain and Caspase-3protein were detected byImmunohistochemical method;The expression of m-Calpain and Caspase-3mRNA were detected by reverse transcription-polymerase chain reaction (RT-PCR). These experiments had reported toand secured its approval from Animal Welfare Committee of Shandong Experimental AnimalCenter (Approved No.:0017145).Results1.The FEV0.3, FEV0.3/FVC and the peak expiratory flow of model group ratsare remarkably lower than those of the control group rats, with statistical significance(P<0.05). The lung tissue of the control group rats is pathologically normal whilethat of the model group rats conspicuously not.2.The mass of the diaphragmatic muscle and long extensor muscle is obviouslylower than that of the control group (P<0.05). The result also indicates distinctabnormal changes in the pathology of the diaphragmatic muscle and long extensormuscle in between the model group and the control group. The muscle apoptosis ratesof diaphragmatic muscle and long extensor muscle in the model group are statisticallysignificantly higher than those of the control group (P<0.05).The muscle apoptosisrates of diaphragmatic muscle and extensor digitorum longus of the tan or brownnuclei in the model group are also apparently higher than the control group.3.The absorbance value of the expression of m-Calpain and Caspase-3of thediaphragmatic muscle and long extensor muscle in the model group is much higherthan that of the control group too(P<0.05). Immunohistochemical sp assay showsthat the expression of m-Calpain and Caspase-3of the model group increasedobviously compared with that of the control group. RT-PCR measurement certifiesthat the expression of m-Calpain and Caspase-3mRNA as well as the absorbancevalue of the diaphragmatic muscle and long extensor muscle in the model group areremarkably higher than those of the control group(P<0.05). ConclusionThe expression of m-Calpain and Caspase-3mRNA in COPD rat skeletal muscle risesremarkably and shows a strong correlation between the two and their positive correlation with themuscle apoptosis rates, thus demonstrating the m-Calpain’s participation in inducing the skeletalmuscle apoptosis of COPD model rats with the help of Caspase-3. | Keywords/Search Tags: | chronic obstructive pulmonary disease, m-Calpain, Caspase-3, skeletal muscleatrophy, cell apoptosis | PDF Full Text Request | Related items |
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