Ginseng Reverses Lung Damage in Asthma

Asthma is a disease of the airways and lungs where airflow both in and out of the lungs is restricted. It is characterized by shortness of breath, wheezing and coughing. Most asthmatics have intermittent "attacks" and are symptom free at other times. Some asthmatics however, are never symptom free. Over time, there is damage to the tissues of the lungs and until now, this damage was thought to be irreversible.

Current asthma therapies such as inhaled steroids are effective in reducing inflammation but do nothing to heal the tissues of the airways. These drugs also have serious side effects such as cataracts, osteoporosis and decreased immune response. New therapeutic options that have fewer side effects and reverse chronic changes in the lungs are essential. This study aimed to determine if oral administration of ginseng would reverse lung histopathology (cell damage).

Mice bred to be prone to chronic asthma were divided into four groups: control, placebo, ginseng, and dexamethasone (a steroid). All mice except those in the control group were sensitized and challenged with ovalbumin. Then, mice in the ginseng group were given 2 gr per kg per day of ginseng and mice in the dexamethasone group received 1 mg/kg per day of dexamethasone for 1 week.

Lung histopathology was evaluated by using light and electron microscopy in all groups. All of the chronic changes of airways in the ginseng group were significantly improved when compared with the placebo group. When compared with the dexamethasone group, the ginseng group had significantly lower numbers of mast cell count. Mast cells are a type of cell which plays a significant role in the inflammatory response of the immune system. Thicknesses of basement membrane, epithelium, and subepithelial smooth muscle were not statistically different between the ginseng and dexamethasone groups. Goblet cell (mucous secreting cells) numbers were much more reduced in the dexamethasone group. The study concluded that ginseng is effective in resolving the established chronic histopathological changes of the lungs in the murine model of asthma.
Sources: http://www.ncbi.nlm.nih.gov/pubmed/18611306

 

 

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