Luteolin alleviates bronchoconstriction and airway hyperreactivity in ovalbumin sensitized mice.
OBJECTIVE
Asthma is an inflammatory disease of the airways and the current focus in managing asthma is the control of inflammation. In this study, we attempted to investigate the anti-asthmatic potential of a plant derived natural compound, luteolin.


METHODS
We used a murine model of airway hyperreactivity, which mimicked some of the characteristic features of asthma. Male BALB/c mice (8-9 weeks) were used for this study.


METHODS
Mice (n = 6) were sensitized by intraperitoneal (i. p.) injection of 10 mg of ovalbumin (OVA) on days 0, 7 and 14 followed by aerosol inhalation (5% OVA) treatments daily beginning from day 19 to day 23. To study its preventive effect, luteolin (0.1, 1.0, and 10 mg/kg body weight; daily) was administered orally during the entire period (0 to 23 day) of sensitization. To study its curative effect, mice were first sensitized and then luteolin (1.0 mg/kg body weight daily) was given orally from day 26 to 32. The airway hyperreactivity, immunoglobulin E (IgE) in the sera, and cytokines (IFN-gamma, IL-4 and IL-5) in the bronchoalveolar lavage fluid (BALF) were measured.


RESULTS
Both during sensitization and after sensitization, luteolin, at a dose of 0.1 mg/kg body weight, significantly modulated OVA-induced airway bronchoconstriction and bronchial hyperreactivity (p < 0.05). Luteolin also reduced OVA-specific IgE levels in the sera, increased interferon gamma (IFN-gamma) levels and decreased the interleukin-4 (IL-4) and interleukin-5 (IL-5) levels in the BALF.


CONCLUSIONS
Our study showed that luteolin treatment during and after sensitization significantly attenuated the asthmatic features in experimental mice. Therefore, luteolin could be used either as a lead molecule to identify an effective antiasthma therapy or as a means to identify novel anti-asthma targets.
Das
M
M
Molecular Immunology and Immunogenetics Lab, Centre for Biochemical Technology, Mall Road, Delhi 110007, India,
Ram
A
A
Ghosh
B
B
D000403:Airway Resistance / Q000502:physiology; D000818:Animals; D001249:Asthma / Q000188:drug therapy / Q000503:physiopathology; D016535:Bronchial Hyperreactivity / Q000188:drug therapy* / Q000503:physiopathology; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D016084:Bronchoconstriction / Q000187:drug effects*; D005100:Expectorants / Q000627:therapeutic use*; D005419:Flavonoids / Q000627:therapeutic use*; D007073:Immunoglobulin E / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D047311:Luteolin; D008297:Male; D016210:Methacholine Chloride / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D018721:Muscarinic Agonists / Q000494:pharmacology; D010047:Ovalbumin / Q000276:immunology*
D005100:Expectorants; D005419:Flavonoids; D015848:Interleukin-5; D018721:Muscarinic Agonists; D016210:Methacholine Chloride; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma; D010047:Ovalbumin; D047311:Luteolin