Vulnerability of Gastric Mucosa to Prednisolone in Rats Chronically Exposed to Cigarette Smoke

Abstract

Abstract. We examined gastric mucosal vulnerability in a rat model of chronic obstructive pulmonary disease (COPD). Male Wistar rats were exposed to cigarette smoke for 12 weeks (CSE rats), and on the last 4 days of exposure, prednisolone was given to induce gastric mucosal injury. Histopathology, pulmonary function, arterial blood gases, and levels of lipid peroxides (LPO), prostaglandin E 2 (PGE 2 ), hypoxia-inducible factor 1 alpha subunit (HIF-1α), and vascular endothelial growth factor (VEGF) in gastric mucosa were examined. We also tested the effect of rebamipide on prednisolone-induced gastric lesions. In CSE rats, although no gastric lesions were detected, LPO, PGE 2 , HIF-1α, and VEGF levels were higher than in control rats. Prednisolone induced gastric hemorrhagic lesions more readily in CSE rats than controls, with concomitant decrease in PaO 2 and increased levels of LPO, HIF-1α, and VEGF. Rebamipide reversed gastric lesions without affecting any parameters examined. CSE rats were found to be a useful animal model of COPD, and COPD appeared to render the gastric mucosa vulnerable to prednisolone.

MTA1 expression correlates significantly with cigarette smoke in non-small cell lung cancer

“…They found the increased HIF-1α and VEGF expression in NSCLC cells after the treatment of nicotine [22]. Takeuchi et al reported that the levels of HIF-1α had been increased after the male Wistar rats were exposed to cigarette smoke for 12 weeks (CSE rats) [23]. Moon HE revealed that MTA1 has deacetylation activity on HIF-1α in vivo by immunoprecipitation and acetylation assays, and MTA1 increased the transcriptional activity of HIF-1α by stabilization of the HIF-1α protein [24].…”

Protective Effect of Demethylation Treatment on Cigarette Smoke Extract–Induced Mouse Emphysema Model

“…Cigarette smoke (CS) is considered to be the primary risk factor for the development of pulmonary emphysema (4). CS contains greater than 1014 free radicals, including reactive oxygen and reactive nitrogen species per puff, which impose a strong oxidative burden resulting in an oxidant/antioxidant imbalance (5).…”

Zl-n-91, a selective phosphodiesterase 4 inhibitor, suppresses inflammatory response in a COPD-like rat model

“…The doses of rolipram and dexamethasone were used in the present study based on our preliminary results and previous studies [14,15]. CS and LPS treatment was performed as follows: rats were confined in a container made of plexiglass (85 cm× 85 cm× 45 cm), and pump CS from 12 standard cigarettes into the container, and rats were exposed to the smoking for 20 min, twice a day with an interval of 15 min and 6 days per week, LPS was administrated intratracheally every 4 weeks at a dose of 1 mg/kg, it took 12 weeks to establish a rat COPD-like animal model [16][17][18][19]. Zl-n-91, rolipram and dexamethasone were diluted in 60% Polyethylene glycol and administrated intraperitoneally for 8 weeks from the fifth week.…”