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Triphala (PADMA) extract alleviates bronchial hyperreactivity in a mouse model through liver and spleen immune modulation and increased anti-oxidative effects
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Objectives: Triphala (TRP), a herbal extract from Tibetan medicine, has been shown to affect lymphocytes and natural killer T (NKT) cell function. We hypothesize that TRP could ameliorate bronchial hyperreactivity through immune-cell modulations. Methods: Asthma mouse models were generated through intraperitoneal (IP) injections of ovalbumin (OVA)/2 weeks followed by repeated intranasal OVA challenges. Mice were then treated with normal saline (OVA/NS) or Triphala (OVA/TRP). Data were compared with mice treated with inhaled budesonide. All groups were assessed for allergen-induced hyperreactivity; lymphocytes from lungs, livers and spleens were analyzed for OVA-induced proliferation and their alterations were determined by flow cytometry. Oxidative reactivity using chemiluminescence, serum anti-OVA antibodies level and lung histology were assessed. Results: Both TRP and budesonide significantly ameliorated functional and histological OVA-induced bronchial hyperreactivity. TRP had no effect on serum anti-OVA antibodies as compared with decreased levels following budesonide treatment. Furthermore, a significant increase in lung and spleen CD4 counts and a decrease in the liver were noted after TRP treatments. Bronchoalveolar fluid from TRP-treated animals but not from the budesonide-treated animals showed anti-oxidative effects. Conclusion: TRP and budesonide caused a significant decrease in bronchial reactivity. TRP treatment altered immune-cell distributions and showed anti-oxidative properties. These findings suggest that immune-cell modulation with TRP can ameliorate lung injury.
Title: Triphala (PADMA) extract alleviates bronchial hyperreactivity in a mouse model through liver and spleen immune modulation and increased anti-oxidative effects
Description:
Objectives: Triphala (TRP), a herbal extract from Tibetan medicine, has been shown to affect lymphocytes and natural killer T (NKT) cell function.
We hypothesize that TRP could ameliorate bronchial hyperreactivity through immune-cell modulations.
Methods: Asthma mouse models were generated through intraperitoneal (IP) injections of ovalbumin (OVA)/2 weeks followed by repeated intranasal OVA challenges.
Mice were then treated with normal saline (OVA/NS) or Triphala (OVA/TRP).
Data were compared with mice treated with inhaled budesonide.
All groups were assessed for allergen-induced hyperreactivity; lymphocytes from lungs, livers and spleens were analyzed for OVA-induced proliferation and their alterations were determined by flow cytometry.
Oxidative reactivity using chemiluminescence, serum anti-OVA antibodies level and lung histology were assessed.
Results: Both TRP and budesonide significantly ameliorated functional and histological OVA-induced bronchial hyperreactivity.
TRP had no effect on serum anti-OVA antibodies as compared with decreased levels following budesonide treatment.
Furthermore, a significant increase in lung and spleen CD4 counts and a decrease in the liver were noted after TRP treatments.
Bronchoalveolar fluid from TRP-treated animals but not from the budesonide-treated animals showed anti-oxidative effects.
Conclusion: TRP and budesonide caused a significant decrease in bronchial reactivity.
TRP treatment altered immune-cell distributions and showed anti-oxidative properties.
These findings suggest that immune-cell modulation with TRP can ameliorate lung injury.
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