The renin-angiotensin system (RAS)was potentially implicated in the pathogenesis of pulmonary disorders through its involvement in inducing pro-inflammatory mediators in the lung tissues. The present study evaluates the effects of the angiotensin receptor blockers (ARBs), telmisartan and valsartan, on the histological changes of lung tissues in sensitized rats. Twenty-fourWister female rats were randomly divided into four groups: A, negative control; B, valsartan-treated group; C, telmisartan-treated group and D, positive control. The rats in the groups B-D were sensitized and challenged with ovalbumin (OVA). Group A rats were sensitized and challenged with normal saline. Rats from groups B and C were treated with either valsartan or telmisartan (5mg/kg/day), respectively. The effects of administered ARBs on lung tissue structures were histologically evaluated. Treatment with telmisartan significantly attenuates the inflammatory and the hyper-proliferative changes in lung tissue after OVA-challenge, while valsartan did not show such effect. In conclusion, telmisartan demonstrates anti-inflammatory and anti-proliferative activities in sensitized rats, while valsartan lacks these effects.
This study was carried out to evaluate the anti-inflammatory effect of losartan in 18 female rats which were divided into 3 groups. Respiratory disease were experimentally induced by the intraperitoneal injection and spray inhalation of ovalbumin (OVA) in first and second group while third group left as negative control group. First group were treated with losartan orally at dose rate of 5 mg/kg body weight, on the other hand second group considered as positive control group. ELISA test were used to estimate the concentration of TNF-α, IL-4 in BALF and total IgE in serum samples. Total WBC, neutrophil, eosinophil and lymphocyte were counted in bronchoaleveolar lavage (BAL). First and second rat groups show signs of pulmonary disease. Losartan treated group showed significant (p<0.05) decrease in concentration of TNF-α (152.483 pg/ml), IL-4 (39.733 pg/ml) in BALF and total serum IgE (56.006 pg/ml) in comparison with positive control group. A significant decrease (p<0.05) were also detected for total WBC (101.33 x10 3), neutrophil (8.83 x10 3), eosinophil (15.50 x10 3) and lymphocytes (15 x10 3) in BALF of losartan treated rat group in compare to positive control group.
Background: Inflammatory airway disease is a well-known worldwide health problem. Available medication is accompanied by dangerous side effects and only provides temporary symptom control. Aim: To investigate the effect of tamsulosin, on the pro-inflammatory cytokines IL-4, IL-6, and TNF-α that are associated with airway inflammation. Method: male, albino rats (n=30), weighing (150-250 gm) were allocated into (5) groups, each group with (6) rats; Group A: normal control group, rats were given distilled water for 14 days. Group B: negative control group, rats exposed to airway sensitization only. Group C: positive control group, treated with prednisolone (4.12mg/kg/d) orally plus airway sensitization. Group D: treated control group with tamsulosin (35 mcg/kg/d) orally plus airway sensitization. Group E: treated control group with tamsulosin (17.5 mcg/kg/d) orally plus airway sensitization. Measurement of inflammatory cytokines IL- 4, IL-6, and TNF-αin serum samples by ELISA. Results: there was a significant reduction (P-value<0.05) of IL- 4 and TNF-α in serum for tamsulosin treated group (D) and group (E) when compared with the positive control group (B). But only group(D) 35mcg/kg/d tamsulosin showed significant reduction(P-value<0.05) in IL-6 level when compared with positive control group (B). Conclusion: Tamsulosin has an anti-inflammatory effect by reduction of IL-4, IL-6, and TNF-α in the rat airway model.
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