NCB-02 (standardized Curcumin preparation) protects dinitrochlorobenzene-induced colitis through down-regulation of NFκ-B and iNOS

AIM： To evaluate the efficacy and mechanism of action of NCB-02, a standardized Curcumin preparation, against 2, 4-dinitrochlorobenzene （DNCB）-induced ulcerative colitis in rats. METHODS： Ulcerative colitis was induced in male rats by sensitizing with topical application of DNCB in acetone for 14 d and intra-colonol challenge with DNCB on day 15. A separate group of animals with vehicle treatment in similar fashion served as control group. Colitis rats were divided into different groups and treated with NCB-02 at doses of 25, 50 and 100 mg/kg b.wt p.o. for 10 d. Sulfasalazine at a dose of 100 mg/kg b.wt for 10 d served as a reference group. On day 10 after respective assigned treatment, all the animals were euthanized and the length of the colon, weight of entire colon and distal 8 cm of the colon were recorded. The distal part of the colon was immediately observed under a stereomicroscope and the degree of damage was scored. Further distal 8 cm of the colon was subject to the determination of colonic myeloperoxidase （MPO）, lipid peroxidation （LPO） and alkaline phosphatase （ALP） activities. A small piece of the sample from distal colon of each animal was fixed in 10% neutral buffered formalin and embedded in paraffin wax and sectioned for immunohistochemical examination of NFK-B and iNOS expression. RESULTS： NCB-02 showed a dose dependent protection against DNCB-induced alteration in colon length and weight. NCB-02 treatment also showed a dose dependent protection against the elevated levels of MPO, LPO and ALP, induced by DNCB. NCB-02 demonstrated a significant effect at a dose of 100 mg/kg b.wt., which was almost equipotent to 100 mg/kg b.wt. of sulfasalazine. Treatment with sulfasalazine and curcuminat a dose of 100 mg/kg b.wt. inhibited the DNCB-induced overexpression of NFK-B and iNOS in the colon. CONCLUSION： Curcumin treatment ameliorates colonic damage in DNCB-induced colitic rats, an effect associated with an improvement in intestinal oxidative stress and downregulation of colonic NFκ-B and iNOS expression.

Caraway extract alleviates atopic dermatitis by regulating oxidative stress,suppressing Th2 cells,and upregulating Th1 cells in mice

Objective:To explore the anti-inflammatory and antioxidant effects of caraway on atopic dermatitis(AD)in mice.Methods:AD was induced in two stages,including sensitization and challenge with the application of 2,4 dinitrochlorobenzene 2% and 0.2%,respectively.Clinical symptoms and histological analysis of the skin were assessed.The effects of caraway on oxidant/antioxidant parameters as well as Th1-and Th2-related cytokines were also evaluated.Results:Caraway reduced the severity of dermatitis in AD-induced mice,as evidenced by significant inhibition of Th2-related cytokines(IL-4 and IL-13)and increased Th1-related cytokine(IFN-γ).Additionally,treatment with caraway significantly increased superoxide dismutase and catalase activity and decreased the malondialdehyde level in the serum of AD mice.Furthermore,caraway inhibited the differentiation of Th2 cells while favoring Th1 cell differentiation in the spleen via regulating their master transcription factors GATA3 and T-bet.Conclusions:Caraway could improve AD autoimmune responses and could be considered a potential candidate to treat AD disease.

Oral Cadmium Intake Enhances Contact Allergen-induced Skin Reaction in Rats

Objective The effect of oral cadmium(Cd)intake to influence contact skin allergies was examined,since it is known that Cd is a heavy metal that affects many tissues,including the skin,in which it disturbs homeostasis,thus resulting in inflammation and injury.Methods Male rats were evoked with experimental contact hypersensitivity reaction(CHS)to hapten dinitrochlorobenzene(DNCB),after prolonged(30 day)oral exposure to an environmentally relevant Cd dose(5 ppm).The ear cell population was analyzed with flow cytometry.Cytokine production by ear skin cells and the activity of skin-draining lymph node(DLN)cells were measured using enzyme-linked immunosorbent assay(ELISA).Results Orally acquired Cd(5 ppm)increased CHS intensity only in Dark Agouti(DA)rats by affecting inflammatory responses in both the sensitization(an increase of IFN-γ and IL-17 cytokine production)and challenge(an increase of CD8^(+)and CD4^(+)cell number and TNF,IFN-γ and IL-17 cytokine production)phases.An increased CHS reaction was seen in Albino Oxford(AO)rats only at a high Cd dose(50 ppm),during the challenge phase(an increase of CD8^(+)and CD4^(+)cell number and TNF,IFN-γ and IL-17 cytokine production).Conclusion These novel data indicate that oral Cd intensifies the skin response to sensitizing chemicals such as DNCB.