ABSTRACT
<p><b>OBJECTIVE</b>To investigate the protective effects of beta-carotene in rats against the development of chronic bronchitis induced by cigarette smoking.</p><p><b>METHODS</b>Forty-two Male Wistar rats were randomly divided into three study groups: (1) control (n = 15), animals underwent no treatment; (2) cigarette smoking (n = 15), animals developed chronic bronchitis through long-term cigarette smoking twice a day for 75 d; (3) beta-carotene plus cigarette smoking animals (n = 12) were given 1 ml or 15 mg/kg beta-carotene orally every day just before cigarette smoking. The levels of IL-6, IL-8, NO, superoxide dismutase (SOD) and lipoperoxide (LPO) in serum, bronchoalveolar lavage fluid (BALF) and lung tissue were measured and the pathological changes to lung tissue were analyzed using light microscopy.</p><p><b>RESULTS</b>Long-term cigarette smoking caused an obvious increase in the amount of IL-6, IL-8 and LPO and a sharp decrease in the levels of NO and SOD in smoking animals compared to controls. beta-carotene intake reversed all the changes induced by smoking and alleviated the pathological changes caused by chronic bronchitis.</p><p><b>CONCLUSIONS</b>Quantitative oral intake of beta-carotene had protective effects against chronic bronchitis induced by long-term cigarette smoking, which was associated with the increased production of NO, the clearance of some oxidative free radicals (OFR) and the alleviation of chronic inflammation.</p>
Subject(s)
Animals , Male , Rats , Bronchitis , Blood , Interleukin-6 , Blood , Interleukin-8 , Blood , Nitric Oxide , Blood , Rats, Wistar , Smoking , Superoxide Dismutase , Blood , beta Carotene , PharmacologyABSTRACT
AIM: To investigate the effect of ambroxol on pulmonary and vascular injury in chronically hypoxic rats. METHODS: 36 male Wistar rats were randomly divided into 3 groups: normal control,chronically intermittent hypoxia(CIH) and ambroxol precaution group(AP).The CIH and AP groups were made into the chronically hypoxic models .The mean pulmonary artery pressure(PAPM) and the levels of plasma superoxide dismutase (SOD) and plasma nitric oxide (NO),lipid peroxide(LPO) were determined. The levels of the lung homogenates SOD, LPO, NO and the changes in pulmonary vascular structure were also examined. RESULTS: The levels of plasma and lung homogenates SOD,NO in CIH group were respectively significantly lower than that of normal control and AP group ( P
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AIM: To reproduce hypercapnic models and approach some pathophysiological changes in rats. METHODS: The mixed gases of high concentrated carbon dioxide (8% CO 2, 21% O 2, 71% N 2) were given to wistar rats 7 hours a day for 28 days. The various indexes were compared between control group (group A) and hypercapnic group (group B). RESULTS: The PaCO 2 [(55.90?4.34) mmHg] and the lipid peroxides (LPO) contents in plasma, lung tissue and right ventricle were significantly higher in group B than those in group A ( P
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AIM: To establish a guinea pig asthma model and to evaluate the effect of airway remodeling on airway responsiveness. METHODS: The guinea pig asthma model was established by ovalbumin (OVA) sensitization and challenge repeatedly. Bronchial provocation tests were conducted through intravenous injection of acetylcholine. The airway morphologic parameters were measured by computer image analysis system. White blood cells and the differential count in bronchoalveolar lavage fluid (BALF) were examined. RESULTS: The resistance of airway was increased significantly after 4 weeks of OVA exposure, but the increase disappeared upon prolonged exposure. After 8 weeks of OVA exposure, fiber tissue in large airway was increased, and the thickness of smooth muscle layer of small airway was enlarged, as compared with that in control animals. CONCLUSION: Airway responsiveness has changed after prolonged OVA exposure in guinea pigs. This change is related to airway remodeling. [
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AIM: To investigate the effects of chronic hy poxia and antagonistic effects of aminophylline on airway inflammation and oxida tive lung damage in rats. METHODS: Thirty-four male Wistar rats were randomly divided into three groups: normal control group (n=10); hypoxia group (n=12); aminop hlline-treated group (n=12). The last two groups were both exposed to hypoxi a 7 hours per day for 21 days. The third group was treated with aminophlline (1 00 mg?kg -1?d -1) before exposed to hypoxia. The level of tumor ne c rosis factor (TNF) -?, interleukin (IL)-10, lipid peroxide (LPO) and the activi ty of superoxide dismutase (SOD) were determined in blood and homogenates of lung tissue. RESULTS: Compared to the control group, the levels of TNF-?, IL -10 and LPO were significantly increased (P