Abstract
The study aim was to evaluate the toxic potential of two polyherbal formulation i.e. " PH 1 & PH 2" and scientific validation of their anti-asthmatic use. Acute oral toxicity study as per OECD 425 TG was conducted. For validation of anti-asthmatic claim, in vivo assay named Ovalbumin (OVA)-induced murine method in Wistar rats was used. Eosinophils and IgE antibody were quantified post-administration of low and high doses of the formulations. No mortality was observed in acute toxicity study. Elevated levels of alkaline phosphatase and damaged liver structure indicating the hepatotoxicity were more pronounced in PH 2 treated rats. Congestion in kidney tissue and increased urea level were evident of the nephrotoxic nature of PH 2 in animals. Treatment with selected polyherbal products decreased the MDA level while increasing the SOD and GSH levels in lung tissue homogenates. The maximum decrease in IgE load (3.18 ± 0.08 IU/mL) was found in rats treated with 12 mg/kg dose of PH 1 followed by 100 mg/kg dose of PH 2 (3.44 ± 0.06 IU/mL). It was concluded that both polyherbal formulations had anti-asthmatic activities, however, PH 1 exhibited the liver and kidney toxicity and should be cautiously used.
Highlights
Asthma is generally regarded as the most common chronic inflammatory disorder characterized by the presence of inflammation and bronchial hyper responsiveness that reversibly obstruct airflow (National & Prevention 2007)
It was thought that the stimulus triggers an intricate web of immune responses through activation of type 2 T-helper lymphocytes (Th2) which produces interleukins (IL-4, IL-5, IL-9 and IL13) that leads to the recruitment of eosinophils and production of immunoglobin E (IgE) causing inflammation of the airways (Lemanske & Busse 2010)
The present study showed that both polyherbal formulations reduced eosinophil count and stabilized mast cells through inhibition of IgE antibody formation
Summary
Asthma is generally regarded as the most common chronic inflammatory disorder characterized by the presence of inflammation and bronchial hyper responsiveness that reversibly obstruct airflow (National & Prevention 2007). The aggravated response to airway-narrowing is generally triggered by changes in weather, viral respiratory infections, allergens or exposure to irritants and exercise that leads to repeated symptoms of chest tightness, breathlessness, wheezing or coughing and tend to vary in intensity over time. Asthma being a heterogeneous condition in children and adults shows quite complex phenotypes under multifaceted host-environment interactions. Both allergic (e.g., molds, dust mites, etc.) and non-allergic stimuli (e.g. tobacco smoke, cold air and exercise, etc.) can trigger asthma (Kim & Mazza 2011). It was thought that the stimulus triggers an intricate web of immune responses through activation of type 2 T-helper lymphocytes (Th2) which produces interleukins (IL-4, IL-5, IL-9 and IL13) that leads to the recruitment of eosinophils and production of immunoglobin E (IgE) causing inflammation of the airways (Lemanske & Busse 2010)
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