The Relationship Of Rat’s Emphysema Induced By Different Ways Of Rearing And Tobacco Smoke And The Atherosclerosis Formation

Objective:By observing the degree of emphysema and atherosclerosis, and the serum tumor necrosis factor(TNF)-α, interleukin(IL)-6 and adiponectin(APN) levels of rats, which were fed with ordinary diet, fat-rich diet or limited energy intake diet and exposed to tobacco smoke or room air, we aim to explore the relationship of rat’s emphysema induced by different ways of rearing and tobacco smoke and the atherosclerosis formation, and its possible mechanism. Methods:Forty-eight 6-week clean male SD rats [wight(200±20) g] were randomly divded into normal diet + smoking group, fat-rich diet + smoking group, limited energy intake + smoking group, normal diet group, fat-rich diet group, and limited energy intake group, which were uncovered to room air or tobacco smoke and fed with fat-rich, limited energy intake or ordinary diet. The relevant indices were measured in each groups after 24 weeks. Lee’s index was calculated. MLI and MAN were calculated and the aortic pathology change was observed by the microscope. VEGF and BMP-2 levels were reflected by immunohistochemical method. The serum APN, IL-6 and TNF-α levels were measured in ELISA kits. Results:⑴ Tobacco smoke and different ways of rearing influenced Lee’s index(F values were 27.710, 95.290, respectively; P<0.05), and there were no interactions between them(F values was 0.455, P>0.05). Tobacco smoke made Lee’s index decreasing. In the non-smoking group, Lee’s index in fat-rich diet group(301.64±4.34) were higher than it in normal diet group(290.03±2.59) and limited energy intake group(280.33±7.46), and it in normal diet group were higher than it in limited energy intake group. In the smoking group, Lee’s index in fat-rich diet + smoking group(296.02±3.94) were higher than it in normal diet + smoking group(283.03±5.42) and limited energy intake + smoking group(271.56±2.45), and it in normal diet + smoking group were higher than it in limited energy intake + smoking group. There are clear differences(all P<0.05).⑵Tobacco smoke and different ways of rearing influenced MLI and MAN(F values were 57.077, 17.839, 27.359, 9.422, respectively; P<0.05), and there were both no interactions between them(F values were 3.078, 0.210, respectively; P>0.05). Tobacco smoke made MLI increasing, and MAN decreasing. In smoking group, MLI in limited energy intake + smoking group [(102.71±11.29)μm] was higher than it in fat-rich diet + smoking group [(91.22±6.41)μm] and normal diet + smoking group [(76.33±10.98)μm]. MLI in fat-rich diet + smoking group was higher than it in normal diet + smoking group. MAN in limited energy intake + smoking group [(125.05±22.78)个/mm2] was lower than it in normal diet + smoking group [(163.72±31.04)个/mm2]. There are clear differences(all P<0.05). There are no differences to MAN in limited energy intake + smoking group compared with it in fat-rich diet + smoking group [(150.41±12.54)个/mm2], and to MAN in fat-rich diet + smoking group compared with it in normal diet + smoking group(P>0.05). In the non-smoking group, MLI in limited energy intake group [(74.35±9.93)μm] and fat-rich diet group [(73.55±8.05)μm] was higher than it in normal diet group [(63.40±5.88)μm], MAN in limited energy intake group [(164.44±36.70)个/mm2] was lower than it in normal diet group[(203.95±24.95)个/mm2] and fat-rich diet group [(186.62±13.07)个/mm2], There are clear differences(all P<0.05). There were no differences to MAN in limited energy intake group compared with it in fat-rich diet group, and MAN in normal diet group compared with it in fat-rich diet group(P>0.05).⑶Observating aorta by the microscopic, there was no atherosclerosis and no hyperplasia in non-smoking group, and endothelial cell structure is complete. In smoking group, there was early atherosclersis, endothelial cell edema, and smooth cell migration and proliferation.⑷Tobacco smoke influenced aortic VEGF and BMP-2 levels(F values were 55.370, 72.913, respectively; P<0.05). and different ways of rearing influenced aortic VEGF level(F values was 3.951, P<0.05), and different ways of rearing had no influence to BMP-2 level(F values was 2.766, P>0.05), and there were both no interactions between them(F values were 1.261, 0.436, respectively; P>0.05). Tobacco smoke made aortic VEGF and BMP-2 increasing. In smonking group, aortic VEGF level in fat-rich diet + smoking group [(61.07±7.21)×10-3] was higher than it in normal diet + smoking group [(51.31±7.16)×10-3] and limited energy intake + smoking group [(53.82±5.83)×10-3]. There are clear differences(P<0.05). There was no difference to aortic VEGF level in limited energy intake + smoking group compared with it in normal diet + smoking group(P>0.05).⑸Tobacco smoke and different ways of rearing influenced serum TNF-α and IL-6 levels(F values were 47.310, 7.276,37.405,9.791, respectively; P<0.05), and there were both no interactions between them(F values were 0.413,0.499, respectively; P>0.05). Tobacco smoke made Serum TNF-α and IL-6 levels increasing. In the smoking group, Serum TNF-α level in limited energy intake + smoking group [(164.94±25.83) pg/ml] and fat-rich diet + smoking group [(163.18±26.29)pg/ml] were higher than those in normal diet + smoking group [(129.40±27.10)pg/ml]. Serum IL-6 level in limited energy intake + smoking group [( 232.04±47.72) pg/ml] and fat-rich diet + smoking group [( 224.17±33.82) pg/ml] were higher than those in normal diet + smoking group [( 173.69±30.63) pg/ml]. There are clear differences(P<0.05). There were no difference to serum TNF-α level in limited energy intake + smoking group compared with it fat-rich diet + smoking group, and to serum IL-6 level in limited energy intake + smoking group compared with it fat-rich diet + smoking group(P>0.05).⑹Tobacco smoke and different ways of rearing influenced serum APN level(F values were 7.064, 48.877, respectively; P<0.05), and there were interactions between them(F values was 10.675, P<0.05). In rats fed with normal diet or limited energy intake diet, tobacco smoke made serm APN level increasing. In rats fed with fat-rich diet, tobacco smoke made serm APN level decreasing. In smoking group, serm APN level in fat-rich diet + smoking group [(4.49±0.75)μg/ml] was lower than it in normal diet + smoking group [(8.14±1.17)μg/ml] and limited energy intake + smoking group [(9.21±1.28)μg/ml], and it in normal diet + smoking group was lower than it in limited energy intake + smoking group. There are clear differences(P<0.05). In non-smoking group, serm APN level in limited energy intake + smoking group [(7.68±1.07)μg/ml] was higher than it in fat-rich diet + smoking group[(5.59±0.65)μg/ml] and normal diet + smoking group [(6.29±0.84)μg/ml]. There are clear differences(P<0.05). There was no difference to serm APN level in fat-rich diet group compared with it in normal diet group(P>0.05).⑺ In smoking group, artic VEGF and BMP-2 levels had a positive correlation with MLI, serm TNF-α and IL-6 levels, and an inverse correlation with MAN level(r values were 0.431, 0.471, 0.448,-0.411, 0.449, 0.428, 0.447,-0.442,respectively; P<0.05). Conclusions:Different ways of rearing and tobacco smoke both can influence the formation of emphysema. Emphysema were positively related to the degree of atherosclerosis, and inflammation should be involved.