Abstract
Pneumonia is a common disorder of the respiratory system associated with inflammation. Telmisartan (TEL) has been reported to treat inflammatory-related diseases. The current study aimed to investigate the possible role and action mechanism of telmisartan on lipopolysaccharide (LPS)-induced pneumonia in rats. Forty male Sprague Dawley rats aged 8 weeks were assigned into four groups ad libitum: a control group received saline only, an experimental group received LPS, a group received telmisartan (5 mg/kg), followed by LPS treatment, and a group received telmisartan (10 mg/kg), followed by LPS treatment. The LPS (2 mg/kg) and equal saline were administered intratracheally. Telmisartan was administered orally 5 days before LPS. After LPS treatment for 24 hr, bronchoalveolar lavage fluid (BALF) and serum were collected for the analysis of cell counts and/or cytokines. Lung tissues were used to perform histological examination, to assess oxidative stress levels, and to determine the levels of PPARγ/NF-κB pathway-related proteins. Rats that received LPS treatment exhibited high levels of lung wet/dry ratio, alkaline phosphatase, lactate dehydrogenase, BALF polymorphonuclear leukocytes count, inflammatory cytokines, and oxidative stress. Meanwhile, LPS also resulted in severe interstitial edema and inflammatory cell infiltration. Interestingly, telmisartan by oral administration markedly ameliorated the adverse effects of pneumonia in rats caused by LPS. In addition, western blotting further revealed that telmisartan could activate PPARγ and repress NF-κB (p65). Telmisartan is protective against pneumonia through inhibition of the inflammation and oxidative stress via the PPARγ/NF-κB pathway.
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