The Astaxanthin Effect On The Differential Count Of Inflamatory Cell In Nickel Allergy Balb/c Mice Model

Abstract

Nickel is a material that commonly used in dentistry, but in some individuals, it can cause type IV delayed-type hypersensitivity (DTH) reaction. In this case, DTH reaction pathway involves T cell helper 1 (Th1) activation that stimulates macrophages to release pro-inflammatory cytokine. Meanwhile, astaxanthin (AST) is carotenoid from red algae that has an anti-inflammatory effect by inhibiting inflammatory mediators. Hematology evaluation is one of the evaluation methods for allergies. This investigation aimed to determine the effect of astaxanthin supplementation on the differential count of inflammatory cells in nickel allergy of mice model. Sixteen Balb/C mice were randomly divided into 4 groups: normal group (N), without therapy group (NA), Astaxanthin 12 mg treatment group (Ast12) and Astaxanthin 6 mg treatment group (Ast6). All groups were given an injection of Nickel(II) chloride (NiCl2 ), Complete Freud’s Adjuvant (CFA), and Incomplete Freud’s Adjuvant (IFA) to obtain the nickel allergy model. Analysis of differential count in an inflammatory cell (neutrophil, lymphocyte, monocyte and eosinophil) performed by utilizing flow cytometry, then, the data were analyzed using Univariate Analysis (p<0.05). As the result, there were no any significant differences between groups for neutrophil and lymphocyte showed by One-Way ANOVA test. Kruskal-Wallis test for eosinophil and monocyte also exhibited no significant difference. In sum, astaxanthin supplementation did not have any effect on the differential count of inflammatory cells (neutrophil, lymphocyte, monocyte and eosinophil) in nickel allergy mice model compared to the normal and without therapy ones