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.

OBJECTIVE: Lipophilic polyphenols in fruit beverages can avidly bind to surfaces of microorganisms and to blood cells and to impart upon them enhanced oxidant scavenging abilities (OSA). However, since many of the polyphenols are actually not fully soluble in water, they are therefore not available to act as effective antioxidant agents. We hypothesized that whole saliva, proteins such as albumin and mucin, human red blood cells and platelets, may all increase the "solubility" and availability of lipophilic antioxidant polyphenols thus increasing the OSA of whole saliva. DESIGN: The OSA of whole un-stimulated human saliva, obtained from healthy donors and of combinations among saliva, mucin, blood cells, fruit beverages and reagent polyphenols were quantified by chemiluminescence, DPPH radical and tetrazolium reduction assays. Kinetics of the clearance of polyphenols from saliva after holding in the mouth for 30s of an extract from beverages cinnamon was assayed by the Folin Ciocalteu's and the luminescence assays. RESULTS: OSA of fruit beverages and of reagent polyphenols were markedly increased by whole saliva, mucin and by red blood cells. Polyphenols associated with a cinnamon extract were retained in the oral cavity for several hours as measured by luminescence and Folin reagent techniques. CONCLUSIONS: A new approach to explain the additional role of saliva and salivary proteins and of blood cells as enhancers of OSA of lipophilic polyphenols is presented. This might have a significant importance to assess complex interactions among polyphenols from nutrients, salivary antioxidants, salivary proteins and blood cells extravasated from injure capillaries during infection and inflammation.

The cascade of events that occurs in Alzheimer's disease involving oxidative stress and the reduction in cholinergic transmission can be better addressed by multifunctional drugs than cholinesterase inhibitors alone. For this purpose, we prepared a large number of derivatives of indoline-3-propionic acids and esters. They showed scavenging activity against different radicals in solution and significant protection against cytotoxicity in cardiomyocytes and primary cultures of neuronal cells exposed to H2O2 species and serum deprivation at concentrations ranging from 1 nM to 10 μM depending on the compound. For most of the indoline-3-propionic acid derivatives, introduction of N-methyl-N-ethyl or N-methyl-N-(4-methoxyphenyl) carbamate moieties at positions 4, 6, or 7 conferred both acetyl (AChE) and butyryl (BuChE) cholinesterase inhibitory activities at similar concentrations to those that showed antioxidant activity. The most potent AChE inhibitors were 120 (3-(2-aminoethyl) indolin-4-yl ethyl(methyl)carbamate dihydrochloride) and 94 (3-(3-methoxy-3-oxopropyl)-4-(((4-methoxyphenyl)(methyl) carbamoyl)oxy)indolin-1-ium hydrochloride) with IC50s of 0.4 and 1.2 μM, respectively.