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Journal of Huazhong University of Science and Technology(Medical Sciences) 2007年第5期27卷 505-507页

作者：张劲农郑灵白明 Department of Respiratory Diseases Union Hospital Tongji Medical College Huazhong University of Science and Technology

In order to explore the roles of tumor necrosis factor-α （TNF-α） and vascular endothelial growth factor （VEGF） in the pathogenesis of pulmonary emphysema, male Wistar rats were randomized into group At, group A2.5 and group A4, each with smoke exposure for 1 month, 2.5 months or 4 months, respectively. Group B t, group B2.5 and group B4 were used as non smoking controls at corresponding time points. TNF-α in bronchoalveolar lavage fluid （BALF） and expression of VEGF in lung tissue was determined by ELISA or by SABC immunohistochemistry assay either. Lung slices were stained with hematoxylin and eosin （HE）. Results showed that in animal with smoke exposure the mean linear interceptor （Lm）, an index of pulmonary emphysema and the content of TNF-α in BALF increased gradually, on contrary, the expression of VEGF in lung tissue decreased （P〈0.05）. This phenomenon was not obvious in animals without smoke exposure. Lm was negatively correlated to the VEGF expression （7=--0.81, P〈0.01） and positively correlated to TNF-α concentration （7 = 0.52, P〈0.004）, which implies that smoke exposure decreased the expression of VEGF and increased the expression of TNF-α. It is plausible to speculate that the imbalance of TNF-α and VEGF may play an important role in the pathogenesis of smoke-induced pulmonary emphysema.

关键词： smoke exposure tumor necrosis factor-α vascular endothelial growth factor pulmonary emphysema

Comparison of Serum Adiponectin in Smoke-induced pulmonary emphysema Rats Fed Different Diets

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Chinese Medical Journal 2016年第2期129卷 187-193页

作者： Rui-Ying Wang Hu Liu Li-JuanMa Jian-Ying Xu Department of Respiratory Diseases Shanxi Dayi Hospital Affiliated to Shanxi Medical University Taiyuan Shanxi 030032 China Department of Respiratory Diseases People's Hospital of Salt Lake Valley Yuncheng Shanxi 044000 China

Background： Smoking and body mass index （BMI） are the key risk factors for chronic obstructive pulmonary disease （COPD）. Adiponectin with both anti-inflammatory and pro-inflammatory properties is a vital modulator of inflammatory processes, which is expressed in epithelial cells in the airway in COPD-emphysema. The aim of this study was to examine the effects of adiponectin on tobacco smoke-induced emphysema in rats, which were fed different diets. Methods： Seventy-six adult （6-8 weeks old） male Sprague-Dawley rats （average weight 220 ± 20 g） were exposed to smoke or smoke-free room atmosphere and fed different diets （regular, high-fat, or low-fat diets） for 6 months. The rats were randomly divided into six groups. They are nonsmoke-exposed regular diet （n = 10）, nonsmoke-exposed high-fat diet （n - 14）, nonsmoke-exposed low-fat diet （n = 14）, smoke-exposed regular diet （n = 10）, smoke-exposed high-fat diet （n = 14）, and smoke-exposed low-fat diet groups （n = 14）. A full 23 factorial design was used to evaluate the effect of independent variables on smoke exposure and different rearing methods. Serum adiponectin and inflammatory cytokines were measured by the enzyme-linked immunosorbent assay （ELISA）. Results： Serum adiponectin levels in rats fed low-fat and regular diets exposed to smoke exposure were remarkably higher than that of rats exposed to room air while serum adiponectin levels of fat-rich diet rats exposed to tobacco smoke were lower than that of rats exposed to room air. Compared with regular diet or low-fat diet group, serum adiponectin levels in high-fat diet rats exposed to tobacco smoke were lower （t = 6.932, 11.026; all P 〈 0.001 ）. BMI was inversely correlated with serum adiponectin levels （r = -0.751, P = 0.012）. Serum interleukin 6 （IL-6）, tumor necrosis factor-or （TNF-a）, and 4-hydroxy 2-nonenal （HNE） levels in rats exposed to low-fat or fat-rich diets were remarkably higher than that of rats exposed to normal diets （IL-6, t = 4.196, 3.480; P 〈 0

关键词： Adiponectin Diet pulmonary emphysema Smoke

Prophylactic Anti-inflammation Inhibits Cigarette Smoke-induced emphysema in Guinea Pigs

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2003年第4期23卷 365-368页

作者：张劲农陶晓南谢建敏向敏付薇 Department of Respiratory Diseases

In this study, the effect of prophylactic anti inflammation on the development of smoke induced emphysema was investigated. Young male guinea pigs aged 1.5 - 2 months (weighing 198.3±26.9 g) were randomly divided into 4 groups: group A (cigarette smoke exposure only), group B (cigarette smoke exposure plus pentoxifylline rich (PTX, 10 mg/d) forage feeding), group C (cigarette smoke exposure plus intermittent cortical steroid injection (Triamcinolone acetonide, 3 mg, im, every three weeks) and control group (group D: animals with sham smoke exposure, raised under the same conditions). Animals in group A, B and C were exposed to smoke of cigarettes for 1 to 1.5 h twice a day, 5 days a week. All animals were killed at the 16th week and followed by morphometrical analysis of the midsagittal sectioned lung slices. Smoke exposure of 16 weeks resulted in visible emphysematous development in Group A but not in Group B and C. It was evidenced by the indicator of air space size, mean linear intercept (L m): 120.6±16.0 μm in Group A; 89.8±9.2 μm in Group B and 102.4±17.7 μm in Group C. The average L m in either group B or group C was shorter than that in Group A (ANOVA and Newman Keuls test, F=8.80, P =0.0002) but comparable to that (94.8±13.2 μm) in group D ( P >0.05). It is concluded that long term prophylactic anti inflammation inhibits pulmonary emphysema induced by cigarette smoking in the guinea pigs.

关键词： cigarette smoke pulmonary emphysema prophylactic anti inflammation

A successful case on traditional Chinese fumigation-soaking therapy in treating diabetic peripheral neuropathy

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Neural Regeneration Research 2006年第5期1卷 478-480页

作者： Hongfang Liu Huayang Wu Lizhong Zhang Jinxi Zhao Department of Nephrology and Endochnology Dongzhimen Hospital Affiliated to Beijing University of Traditional Chinese Medicine Beijing 100700 China

AIM： To investigate the scheme of inducing the diabetic peripheral neuropathy （DNP） symptoms by combine Chinese traditional medicine with modern medicine. METHODS： Patient hospitalized on April 1, 2005. Main symptoms in hospitalization： His bilateral fingers and toe tips felt stabbing pain, numb, cold, assuming a type of sock set which alleviated after he had a rest and aggravated after exercise. He had also got the symptom of dizziness, asthenia, eating little food, very thin bowel and body pain which had influence on his sleeping. Physical examination in hospital： The bilateral lower limbs which got a hyperpathia did not swell. The bilateral dorsum pedis artery pulsation was atlenuative. The skin temperature was not high. Other nerve system examination had been discovered abnormal. Diagnosis： Traditional Chinese medical diagnosis： Xiaokebing （blood stasis for insufficiency of qi, blockage of meridian and collaterals）. Modern medical diagnosis： Diabetes type 2, DNP, diabetic lower limbs artery obliteration, diabetic foot （0 level）, diabetic retinopathy, coronary atherosclerotic heart disease, hypertension, chronic bronchitis, chronic obstructive pulmonary emphysema. Carried on the former therapy plan that continued to use insulin to control blood glucose, depressed blood pressure and total plasma lipoprotein etc. Meanwhile used the therapy of bilateral feet medicinal bath （San/ing 30 g, Ezhu 30 g, Ruxiang 30 g, Moyao 30 g, Zhichuanwu 30 g, Zhicaowu 30 g, Weilingxian 30 g, Mugua 30 g, Sangzhi 30 g）, boiled in water, 1 dose everyday, soak feet twice a day, 20-30 minutes once, 〈 37 ℃. RESULTS： Seven days later, the pain of bilateral feet alleviated obviously, and the bilateral dorsum pedis artery pulsation enhanced. Blood glucose and total plasma lipoprotein had no changes. CONCLUSION ： The symptoms of DNP such as pain, coldness, numbness of the lower limbs can be induced by combining feet medicinal bath （fumigation-soaking） treatment with modern medicine.

关键词： medical diagnosis lower limbs diabetic peripheral neuropathy Chinese traditional medicine blood glucose pulmonary emphysema blood pressure heart disease type of

Effects of pentoxifylline on Wnt/β-catenin signaling in mice chronically exposed to cigarette smoke

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Chinese Medical Journal 2010年第19期123卷 2688-2694页

作者： WANG Zheng ZHANG Jin-nong HU Xiao-fei CHEN Xue-lin WANG Xiao-rong ZHAO Ting-ting PENG Mei-jun ZOU Ping Institute of Respiratory Medicine Department of Geriatrics Department of Haematology Affiliated Union Hospital of Huazhong University of Science and Technology Wuhan Hubei 430022 China

Background Previous discovery that long-term administration of pentoxifylline （PTX） to mice chronically exposed to smoke led to the development of pulmonary fibrosis rather than emphysema initiated our curiosity on whether the Wnt/β-catenin pathway, a set of signaling proteins essential to organ development and lung morphogenesis in particular were activated in the pathogenesis of pulmonary fibrosis. Methods Male BALB/c mice were randomized into four study groups： Group Sm, smoke exposure and taken regular forage; Group PTX, no smoke but taken PTX-rich forage; Group Sm＋PTX, smoke exposure and taken PrX-rich forage; Group control： shamed smoke exposure and taken regular forage. Animals were sacrificed at day 120. Morphometry of the lung sections and the expressions of TGF-β1, hydroxyproline, β-catenin, cyclin D1, T cell factor 1 （Tcf-1） and lymphoid enhancer factor 1 （Lef-1） mRNA, etc, in the lung homogenate or in situ were qualitatively or quantitatively analyzed. Results As expected, smoke exposure along with PTX administration for 120 days, lungs of the mice progressed to be a fibrosis-like phenotype, with elevated fibrosis score （3.9±1.1 vs. 1.7±0.6 in Group Sm, P 〈0.05）. TGF-β1（pg/g）（1452.4±465.7 VS. 818.9±2.02.8 in Group Sm, P 〈0.05） and hydroxyproline （mg/g）（5.6±0.6, vs. 2.4±0.1 in Group Sm, P 〈0.05） were also consistently increased. The upregulation of β-catenin measured either by counting the cell with positive staining in microscopic field （17.4±7.9 vs. 9.9±2.9 in Group Sm, P 〈0.05） or by estimation of the proportion of blue-stained area by Masson＇s trichrome （11.8±5.6 vs. 4.7±4 in Group Sm） in Group SM＋PTX was much more noticeable as than those in Group Sm. The expression of β-catenin measured by positive cell counts was correlated to TGF-β1 concentration in lung tissue （r=0.758, P 〈0.001）. PTX per se caused neither fibrosis nor emphysema though expression of β-catenin and downstream gene cyclin D1 may also be altered by this medication. Conclusions PTX

关键词： pentoxifylline Wnt signaling pathway Wnt/β-catenin pulmonaryfibrosis pulmonary emphysema