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Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 197
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File: /var/www/html/application/helpers/my_audit_helper.php
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Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
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Function: simplexml_load_file_from_url
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Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
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Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
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Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
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Function: require_once
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Ethnopharmacological Relevance: Melia azedarach L. is a traditional medicinal plant used to control pain, pyrexia, inflammation and bacterial infections that possesses several pharmacological activities, including anti-inflammatory and antioxidant activities. Particularly, the root of M. azedarach was used as expectorant and anti-cough and asthma treatment. Based its properties, M. azedarach is expected to have a potential to treat allergic asthma, chronic inflammatory respiratory disease. However, there is no study on anti-asthmatic effects of M. azedarach and its mechanism of action until now.
Aim Of The Study: We investigated the active ingredient of M. azedarach fruit extract (MAE) using high-performance liquid chromatography (HPLC) and explored the therapeutic effects of MAE on pulmonary inflammation and mucus hypersecretion using a murine model of ovalbumin (OVA) exposed asthma.
Materials And Methods: The ingredients of MAE were analyzed using HPLC. To develop allergic asthma model, the animals were sensitized (days 1 and 14) and the airway was challenged (from day 21-23) using OVA. MAE was administered by oral gavage once a day from day 18-23 at doses of 30 and 100 mg/kg.
Results: HPLC analysis revealed the presence of toosendanin in MAE. In asthmatic mice, MAE administration effectively suppressed the inflammatory cell counts in bronchoalveolar lavage fluid (BALF) along with a reduction in airway hyperresponsiveness. Moreover, MAE administration inhibited the production of proinflammatory cytokines and immunoglobulin E in BALF and serum of asthmatic mice, respectively. These results were similar to the results of histological examination showing a reduction in pulmonary inflammation and mucus hypersecretion. MAE elevated the expression of nuclear factor erythroid 2-related factor 2, heme oxygenase-1, and superoxide dismutase 2, which in turn resulted in the suppression of matrix metallopeptidase-9 expression in lung tissue of asthmatic mice.
Conclusions: Altogether, MAE successfully inhibited allergic asthma in OVA-exposed mice. Thus, MAE could be a potential therapeutic remedy for treating allergic asthma.
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http://dx.doi.org/10.1016/j.jep.2023.117426 | DOI Listing |