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Objective: To establish a mouse model of chronic obstructive pulmonary disease (COPD) and associated pulmonary hypertension (COPD-PH) induced by nose-only cigarette smoking exposure plus airway lipopolysaccharide (LPS) inhalation., Methods: There were 24 male C57B6 mice divided into a control group and a model group at random. The model group was given LPS by intranasal inhalation on day 1 and day 14 and exposed to the cigarette smoke in a nose-only exposure system, while the control group was given physiological saline and exposed to normal air. The model establishment was evaluated according the following parameters: the lung function and the right heart pressure, the total and differential cell numbers in bronchial alveolar lavage fluid (BALF), and the pathological changes of lung tissues., Results: The functional residual capacity data of the model group and the control group were (0.402 ± 0.057) and (0.243 ± 0.064) ml respectively (P<0.05). The inspiratory resistance data of the model group and the control group were (1.056 ± 0.121) and (0.789 ± 0.063) cmH(2)O · ml(-1) · s(-1) (1 cmH(2)O=0.098 kPa) respectively (P<0.05). The static lung compliance data of the model group and the control group were (0.084 ± 0 .007) and (0.056 ± 0.004) cmH(2)O/ml respectively (P<0.05). The right ventricular mean pressure of the model group and the control group were (11.3 ± 1.3) and (7.9 ± 1.1) mmHg (1 mmHg=0.133 kPa) respectively (P<0.05), while the right ventricular hypertrophy index of the model group and the control group were (0.267 ± 0.019) and (0.195 ± 0.023) respectively (P<0.05). Moreover, the histological staining showed that goblet cell hyperplasia, lung inflammation and thickening of smooth muscle layers of bronchial and pulmonary small vessels occurred in the model group, which indicated ongoing airway and blood vessel remodeling., Conclusions: A COPD-PH mouse model was established by nose-only cigarette smoking exposure plus airway LPS inhalation in a short period of time, and this method was more similar to the smoking behavior of human.

Objective: To investigate the effect of chronic hypoxia on pulmonary vein remodeling in rats and its underlying molecular mechanism., Methods: Totally 20 adult SD rats (200-250 g), in accordance with a random number table, were divided into normoxia control group (NC) and chronic hypoxia group (CH). CH group rats were put into automatic hypoxia box for 21 days. After that, RVSP, mRVP and RV/( LV+S) were measured; Lung histopathological sections were prepared. The lumen area, ratio of wall thickness to radius of pulmonary veins were gauged by using the Image Pro Plus 6.0 software. Primary PVSMCs were cultured in hypoxia (4% O₂) or normoxia (21% O₂) for 60 hours respectively before extracted total protein for Western blotting analysis. PPARγ protein expression in rat pulmonary vein smooth muscle and pulmonary vein smooth muscle cells was detected by Western blot., Results: Compared with NC group [(27.06 ± 2.10), (12.58 ± 0.82) mmHg (1 mmHg=0.133 kPa)], the RVSP and mRVP in CH group [(50.46 ± 9.51), (21.66 ± 1.85)mmHg] were significantly increased (P<0.05). The RV/(LV+S) of CH group was (0.56 ± 0.05), markedly higher than that of NC group (0.36 ± 0.04, P<0.05). The luminal area/total area of vein in CH group decreased to (48.62 ± 13.61)% compared with that in NC group (66.16 ± 8.72)% (P<0.05). The wall thickness/venous radius (WT%) of CH group increased from (7.23 ± 0.71)% (NC) to (16.43 ± 5.08)% (P<0.05). The level of PPARγ protein in pulmonary vein smooth muscle of CH group was (52.95 ± 3.83)%, lower than that of NC (100 ± 0)% (P<0.05). PPARγ protein in pulmonary vein smooth muscle cells cultured in vitro in hypoxia was (59.38 ± 17.12)%, lower than that cultured in normoxia (100 ± 0)% (P<0.05)., Conclusion: Hypoxia induced increase of RVSP, mRVP, RV/(LV+S), and accompanied with pulmonary venous remodeling. The underlying mechanism of the vein change may related to down-regulated expression of PPARγ.

Objective: To investigate the effect of sodium tanshinone IIA sulfonate (STS) on rat right ventricular systolic pressure (RVSP), mean right ventricular pressure (MRVP), right ventricular hypertrophy index [RV/(LV+S)], pulmonary vascular remodeling, and PPARγ protein expression in pulmonary artery smooth muscle of monocrotaline (MCT) induced rat pulmonary hypertension model., Methods: The pulmonary hypertension model was established by subcutaneously injection of MCT, and the rats were treated with or without STS for 21 days. After that, RVSP, mRVP and RV/(LV+S) were measured. Lung histopathological sections were prepared, and the lumen area, the wall thickness and arterial radius of pulmonary arteries were quantified using the Image Pro Plus 6.0 software. PPARγ protein expression in rat pulmonary artery smooth muscle was detected by Western blot., Results: Compared with control group, the RVSP, mRVP were significantly increased in MCT group (P < 0.05), while in the MCT+STS group, it was decreased from (81.2 ± 1.9) and (28.6 ± 2.0) mmHg to (35.4 ± 8.3) and (14.1 ± 5.4) mmHg, respectively (P < 0.05). The RV/(LV+S) of MCT group was (0.57 ± 0.04), markedly higher than those of control group and control+STS group (0.33 ± 0.02) and (0.34 ± 0.02) , respectively, P < 0.05, while in MCT+STS group, the RV/(LV+S) was (0.43 ± 0.02), lower than that of MCT group (P < 0.05) ;The luminal area/total area of MCT group decreased to (27 ± 6)%compared with control rats (56.00 ± 3.00) % (P < 0.05) . The wall thickness/artery radius (WT%) of MCT group increased from (20 ± 4) % (control group) to (40 ± 3) % (P < 0.05) .In MCT+STS treated rats, luminal area/ total area and WT% were (39.0 ± 2.0) %and (31.0 ± 2.0) %, both statistically different from MCT group (P < 0.05) . The level of PPARγ protein in pulmonary artery smooth muscle of MCT group was (48 ± 4) %, lower than control group (100 ± 0) % (P < 0.05) .In the MCT+STS group, PPARγ protein expression was recovered (102 ± 3) %, (P < 0.05) ., Conclusion: STS markedly decreased RVSP,MRVP, RV/(LV+S) and pulmonary vascular remodeling in MCT induced pulmonary hypertension rat, and PPARγ might be targeted as a key molecule during STS treatment.

Background and Objective: Transient receptor potential canonical (TRPC) proteins, a group of Ca2' permeable nonselective cation channels, are thought to constitute store-operated calcium channels (SOCC) and mediate store-operated calcium entry (SOCE) in various cell types. Members of TRPC have been found to be involved in abnormal proliferation, differentiation, and growth of cancer cells. The aim of this study is to detect the mRNA and protein expression of TRPC in non-small cell lung cancer (NSCLC)., Methods: Real-time quantitative PCRwas performed to screen the expression of TRPC mRNA in NSCLC tissue. Protein expression of TRPC was detected by Western blot., Results: Among the seven family members of TRPC so far identified (TRPC1-7), we detected the expression ofTRPC1, TRPC3, TRPC4, TRPC6 mRNA in 24 cases of NSCLC tissue; TRPC2, TRPC5 and TRPC7 mRNA were not detectable. The relative abundance of the expressed TRPC was TRPC1 approximately equal TRPC6 > TRPC3 > TRPC4. Western blot confirmed the protein expression of TRPC1, TRPC3, TRPC4 and TRPC6 in NSCLC tissue., Conclusion: Out of the seven members of TRPC, we found TRPC1, TRPC3, TRPC4, TRPC6 mRNA and protein were selectively expressed in human NSCLC tissue. This study could provide a basis for future exploration of the individual role of these TRPC proteins in mediating SOCE and in the progression of lung cancer.