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Objective To investigate the effects of mitochondrial DNA (mtDNA) copy number in peripheral blood and related factors on the risk of hypertension in coal miners.Methods A case-control study was conducted in 378 coal miners with hypertension and 325 healthy coal miners recruited from Datong Coal Mine Group.A standard questionnaire was used to collect their general information,such as demographic characteristics,habits and occupational history.Fluorescence quantitative PCR was performed to detect the copy number of mtDNA.Logistic regression model was applied for identifying the related risk factors of hypertension and analyzing the interaction between mtDNA copy number and risk factors.Results The prevalence of hypertension of high mtDNA copy number was lower than mtDNA copy numberin 0-5.67 group,but the difference was not statistically significant (P=0.414).Alcohol drinking (OR=1.80,95％CI:1.26-2.56),family history of hypertension (OR=1.74,95％ CI:1.20-2.50),work shifts (OR=0.69,95％ CI:0.48-0.99),education level (P=0.012) and family monthly income level (P=0.001) were related to the prevalence of hypertension.There were potential interactions between mtDNA copy number and alcohol drinking,family monthly income level,family history of hypertension,respectively.Alcohol drinking was a risk factor for hypertension [1.77(1.25-2.50)].Potential interactions between mtDNA copy number and alcohol drinking reduced the risk of hypertension (OR=1.20,95％CI:1.07-1.35).Family history of hypertension was a risk factor for hypertension [1.81(1.26-2.59)].Potential interactions between mtDNA copy number and family history of hypertension reduced the risk of hypertension (OR=1.24,95％ CI:1.09-1.41).Family monthly income level was a protect factor for hypertension [0.55(0.46-0.66)].Potential interactions between mtDNA copy number and family monthly income level increased the protection role of hypertension (OR=0.90,95％CI:0.86-0.94).Conclusion mtDNA copy number variation was not significantly associated with the prevalence of hypertension in coal miners,but mtDNA copy number shewed multiplication interaction on the prevalence of hypertension with alcohol drinking,family monthly income level as well as family history of hypertension and made their influences weaken.
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Objective To investigate the effects of mitochondrial DNA (mtDNA) copy number in peripheral blood and related factors on the risk of hypertension in coal miners.Methods A case-control study was conducted in 378 coal miners with hypertension and 325 healthy coal miners recruited from Datong Coal Mine Group.A standard questionnaire was used to collect their general information,such as demographic characteristics,habits and occupational history.Fluorescence quantitative PCR was performed to detect the copy number of mtDNA.Logistic regression model was applied for identifying the related risk factors of hypertension and analyzing the interaction between mtDNA copy number and risk factors.Results The prevalence of hypertension of high mtDNA copy number was lower than mtDNA copy numberin 0-5.67 group,but the difference was not statistically significant (P=0.414).Alcohol drinking (OR=1.80,95％CI:1.26-2.56),family history of hypertension (OR=1.74,95％ CI:1.20-2.50),work shifts (OR=0.69,95％ CI:0.48-0.99),education level (P=0.012) and family monthly income level (P=0.001) were related to the prevalence of hypertension.There were potential interactions between mtDNA copy number and alcohol drinking,family monthly income level,family history of hypertension,respectively.Alcohol drinking was a risk factor for hypertension [1.77(1.25-2.50)].Potential interactions between mtDNA copy number and alcohol drinking reduced the risk of hypertension (OR=1.20,95％CI:1.07-1.35).Family history of hypertension was a risk factor for hypertension [1.81(1.26-2.59)].Potential interactions between mtDNA copy number and family history of hypertension reduced the risk of hypertension (OR=1.24,95％ CI:1.09-1.41).Family monthly income level was a protect factor for hypertension [0.55(0.46-0.66)].Potential interactions between mtDNA copy number and family monthly income level increased the protection role of hypertension (OR=0.90,95％CI:0.86-0.94).Conclusion mtDNA copy number variation was not significantly associated with the prevalence of hypertension in coal miners,but mtDNA copy number shewed multiplication interaction on the prevalence of hypertension with alcohol drinking,family monthly income level as well as family history of hypertension and made their influences weaken.
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Objective α?Asarone has the effect of relieving cough and asthma as well as sedative, hypnotic and anticonvul?sive function. Our study was designed to explore the effects of apoptosis induced by α? Asarone on human esophageal carcinoma Eca?109 cell line as well as the expression levels of GADD153 and Smac mRNA. Methods Human esophageal carcinoma Eca?109 cells were cultured in vitro, which were divided into blank control group, 5?FU group( 500μg/mL) andα?Asarone group of different dosages ( 25,50,100μg/mL) . After cultivation, MTT method and Annexin V?PI were used to measure cell proliferation rate and apoptosis rate. Expression levels of GADD153 and Smac protein and mRNA were detected by western blotting and real? time quantitative PCR. Results Compared with blank control group, the cell proliferation rates in other groups decreased significantly (P<0.01), and cell apoptosis rate increased significantly ( P<0.01) . Compared with blank control group, the expression levels of GADD153 and Smac pro?tein and mRNA in other groups increased significantly( P<0.05) . Conclusion α? Asarone can inhibit cell proliferation and induce the apoptosis of human esophageal carcinoma Eca?109 by regulating the expression levels of GADD153 and Smac gene.
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@#ObjectiveTo evaluate the quantitative and qualitative changes of peripheral-type benzodiazepine recepors (PBRs) in brain mitochodria and in platelet membrane in aging rats. MethodsMale Sprague-Dawley rats were divided into 3- and 24-month groups. All animals were sacrificed by decapitation and the brains were immediately removed. Mitochondrial components from dissected cerebral cortex were isolated. The membrane of platelets from venous blood was prepared by the method of hypotonic hemolysis. The specific binding assay of the radioactive PBRs antagonist ［3H］PK11195 to membrane was performed. Scatchard analysis was performed to estimate the equilibrium dissociation constant (Kd) and the maximal binding site density (Bmax). ResultsA significant increase in ［3H］PK11195 binding activity in the mitochodria from cerebral cortex in 24-month rats was observed compared to that in 3-month rats(P<0-001). Meanwhile, the Scatchard analysis revealed that there was an increase in Bmax, with a significant increase in Kd in 24-month rats. The same change of ［3H］PK11195 binding activity was noted for platelet membrane in 24-month rats(P<0-001).ConclusionThe density of PBRs increases in cortex mitochondria in aging rats, but the binding affinity of PBRs decreases which may be attributable to the progressive pathogenesis of aging in rats. ［3H］ PK11195 binding activity of platelet membrane might reflect the change of PBRs in the brain tissue.
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0.05).After reperfusion,Sevo group and Post group resulted in a significant increase(P