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Background: Allergic asthma is a inflammatory disease defined as a condition of chronic airway inflammation. Asthma can be provoked by various stimuli like allergens inhalation like dust particles, pollen, and pollutants in the air. Objective: This exploration was dedicated to investigate the anti-asthmatic properties of tilianin against the ovalbumin (OVA)-initiated asthma in mice.MethodologyThe asthma was provoked to the mice via administering 100 μl of aluminum hydroxide containing 20 μg of OVA and treated with the 10 and 20 mg/kg of tilianin, respectively. The levels of Th2 cytokines, OVA-specific IgE, eotaxin, pro-inflammatory mediators, antioxidants, and other markers were inspected by marker specific assay kits. The mRNA expressions of TGF-β1, Smad, iNOS, and COX-2 was assessed using RT-PCR analysis. The lung histology was analyzed microscopically to detect the histological changes. Results: Tilianin treatment remarkably suppressed the IL-4, IL-5, and IL-13, IFN-γ, eotaxin, and IgE levels. The NO, MPO, and inflammatory makers TNF-α, IL-6, IL-12, and TXB2 was substantially diminished by the tilianin treatment. The TGF-β1, iNOS, and COX-2 expressions were appreciably suppressed by the tilianin. The histological findings proved that the tilianin treatment alleviated the OVA-provoked histopathological changes in the lung tissues. Conclusion: Our findings proved that tilianin effectively alleviated the OVA-provoked asthma in animals and it could be a talented anti-asthmatic candidate.

Metformin has been involved in modulating inflammatory state and inhibiting cell proliferation and angiogenesis. This study aimed to determine whether metformin alleviates airway inflammation and remodeling of experimental allergic asthma and elucidate the underlying mechanism. We sensitized and challenged mice with ovalbumin (OVA) to induce allergic asthma. During the challenge period, metformin was administered by intraperitoneal injection. By histopathological and immunohistochemical analyses, metformin-treated mice showed a significant alleviation in airway inflammation, and in the parameters of airway remodeling including goblet cell hyperplasia, collagen deposition and airway smooth muscle hypertrophy compared to those in the OVA-challenged mice. We also observed elevated levels of multiple cytokines (IL-4, IL-5, IL-13, TNF-α, TGF- β 1 and MMP-9) in the bronchoalveolar lavage fluid, OVA-specific IgE in the serum and angiogenesis-related factors (VEGF, SDF-1 and CXCR4) in the plasma from asthmatic mice, while metformin reduced all these parameters. Additionally, the activity of 5′-adenosine monophosphate-activated protein kinase a (AMPK α) in the lungs from OVA-challenged mice was remarkably lower than control ones, while after metformin treatment, the ratio of p -AMPK α to AMPK α was upregulated and new blood vessels in the sub-epithelial area as evidenced by CD31 staining were effectively suppressed. These results indicate that metformin ameliorates airway inflammation and remodeling in an OVA-induced chronic asthmatic model and its protective role could be associated with the restoration of AMPK α activity and decreased asthma-related angiogenesis. [ABSTRACT FROM AUTHOR]