The Blend of Taurine and Aloe Vera Extract Boosts Action Against Skin Irritation: In Vitro and Clinical Evaluations.

Regular usage of cosmetic products and drugs in dermatological vehicles may cause irritant contact dermatitis. For example, aluminum chloride (AlCl3), the most efficacious antiperspirant salt to treat hyperhidrosis, shows high irritancy potential. To mitigate the irritant contact dermatitis caused by topical application of products containing AlCl3, we investigated the anti-irritating effects of aloe extract and taurine in vitro and in vivo. In an in vitro experiment, reconstructed human epidermis model, EpiDerm, was tested with AlCl3 in the presence or absence of taurine and aloe extract. In a human clinical study, 12 adult subjects were tested with two products, a commercial AlCl3 antiperspirant product and a prototype 12% AlCl3 formulation containing 0.1% taurine and 0.1% aloe extract. Skin irritation potential in vitro and in vivo was measured by the release of pro-inflammatory cytokine, IL-1α, and chemokine, IL-8. Taurine and aloe extract significantly (p < 0.05) reduced IL-lα and IL-8 production in vitro and in vivo after topical application of formulations containing AlCl3. The blend of taurine and aloe extract demonstrated boosted anti-irritation benefits on AlCl3 irritated skin both in vitro and in vivo. These results suggest that the combination of these anti-irritating actives may possibly be effective in mitigating irritant contact dermatitis caused by other dermatological vehicles containing irritating agents, but further research is warranted to assess their effects.

Alleviation of dimethylnitrosamine-induced liver injury and fibrosis by betaine supplementation in rats.

Previous studies suggested that betaine intake might antagonize the induction of oxidative stress-mediated acute liver injury through regulation of the sulfur-amino acid metabolism. In this study we examined the protective effects of betaine on chronic liver injury and fibrosis induced by dimethylnitrosamine (DMN). Male rats were supplemented with betaine (1%, w/v) in drinking water from 2 weeks prior to the initiation of DMN treatment (10mg/(kg day), i.p., 3 days/week, for 1, 2, or 4 weeks) until sacrifice. Induction of liver injury was determined by quantifying serum alanine aminotransferase, aspartate aminotransferase activities, bilirubin levels, hepatic xenobiotic-metabolizing capacity, histopathological changes and 4-hydroxyproline levels. Development of oxidative injury was estimated by malondialdehyde (MDA) levels and total oxyradical scavenging capacity (TOSC) of liver and serum toward hydroxyl, peroxyl radicals, and peroxynitrite. Progressive changes in the parameters of liver injury and fibrosis were evident in the rats challenged with DMN. Elevation of MDA levels in liver was significant before the onset of a change in any parameters determined in this study. Betaine supplementation markedly attenuated the induction of hepatotoxicity and fibrosis by DMN. Elevation of MDA and the reduction of TOSC were also depressed significantly. Development of liver injury corresponded well with the induction of oxidative stress in rats treated with DMN, both of which are inhibited effectively by betaine supplementation. It is suggested that betaine may protect liver from fibrogenesis by maintaining the cellular antioxidant capacity.