curcumin and Dermatitis--Contact

This review focuses on contact dermatitis as an adverse effect of a selection of topically used herbal medicinal products for which the European Medicines Agency has completed an evaluation up to the end of November 2013 and for which a Community herbal monograph has been produced. Part 1: Achillea millefolium L.-Curcuma longa L.

Topics: Achillea; Aesculus; Aloe; Arctium; Calendula; Cinnamomum zeylanicum; Commiphora; Curcuma; Dermatitis, Contact; Humans; Phytotherapy; Plant Extracts; Plant Preparations

Contact urticaria (CU) defines the weal-and-flare reaction that occurs after external cutaneous contact with a causative agent. These reactions often cause discomfort for patients, affect their quality of life, and in severe cases may be life-threatening. Some dyes are known to be urticariogens. Many people have daily exposure to these urticariogens, because of the widespread use of dyes, for example in textiles, cosmetics and foods. We reviewed industrial and cosmetic dyes such as hair dyes, basic blue 99 dye, patent blue dyes, henna, red dyes, curcumin and reactive dyes, which can potentially cause CU. Overall, the reported cases of CU lacked appropriate controls. Hair-dye constituents such as preservatives and intensifiers may play an important role as causative agents of CU. We recommend appropriate protection guidelines to reduce the incidence of CU in high-risk groups such as hairdressers, dye-factory workers or workers in dye-related industries.

Topics: Coloring Agents; Cosmetics; Curcumin; Dermatitis, Contact; Humans; Naphthoquinones; Patch Tests; Quaternary Ammonium Compounds; Time Factors; Urticaria

Irritant contact dermatitis (ICD) and hyperpigmentation are the problems associated with skin. Topical curcumin (CUR) although effective in hyperpigmentation and ICD, is a challenging molecule due to low-solubility. Encapsulation of CUR into solid lipid nanoparticles (SLNs) makes it amenable to topical dosing as their small size promotes its penetration into the skin. CUR-SLNs were prepared using Precirol ATO5 and Tween-80 by probe ultrasonication method. Further, CUR-SLNs were incorporated into Carbopol gel and investigated for ex-vivo skin permeation, skin deposition and skin irritation studies. The potential of CUR-SLN gel was checked against hyperpigmentation through the inhibition of tyrosinase enzyme. It was further evaluated for possible effects on ICD using BALB/c mice. The optimized CUR-SLN showed the particle size of 51 nm and 93% EE. Ex vivo permeation of CUR-SLN gel exhibited controlled drug release up to 24 h, similarly in vitro drug deposition studies showed potential for skin targeting. In vitro tyrosinase inhibition assay indicates that the formulated gel has potential in skin depigmentation. The gel also confirmed proficient suppression of ear swelling and reduction in skin water content in the BALB/c mouse. Thus, the CUR-SLN gel would be a safe and effective alternative to conventional vehicles for treatment of ICD and pigmentation.

Topics: Administration, Topical; Animals; Curcumin; Dermatitis, Contact; Diffusion; Drug Carriers; Gels; Hyperpigmentation; Irritants; Lipids; Mice; Monophenol Monooxygenase; Nanoparticles; Skin; Solubility

Psoriasis is a chronic autoimmune human skin disorder that is characterized by excessive proliferation of keratinocytes, scaly plaques, severe inflammation and erythema. The pathophysiology of psoriasis involves interplay between epidermal keratinocytes, T lymphocytes, leukocytes and vascular endothelium. Increased leukocyte recruitment and elevated levels of cytokines, growth factors and genetic factors like interleukin (IL)-1β, IL-6, IL-17, IL-22, IL-23, tumour necrosis factor (TNF)-α, interferon (IFN)-γ, transforming growth factor (TGF)-β, toll-like receptor (TLR)-2, signal transducer and activator of transcription (STAT-3), 15-lipoxygenase (LOX)-2, coiled-coil alpha-helical rod protein 1 (CCHCR1), steroidogenic acute regulatory protein (StAR) and vitamin D receptor (VDR) are the most critical factors governing the exacerbation of psoriasis. In the present study, an attempt was made to elucidate the preventive role of herbal extracts of four dermo-protective Ayurvedic plants, Tinospora cordifolia (TC), Curcuma longa (CL), Celastrus paniculatus (CP) and Aloe vera (AV), against psoriasis-like dermatitis. Parkes (P) strain mice were initially induced with psoriasis-like dermatitis using topical application of imiquimod (IMQ, 5 %), followed by subsequent treatment with the herbal extracts to examine their curative effect on the psoriasis-like dermatitis-induced mice. The extracts were orally/topically administered to mice according to their ED/LD50 doses. Phenotypical observations, histological examinations, and semi-quantitative reverse transcription PCR (RT-PCR) analyses of the skin and blood samples of the control, IMQ-treated and herbal extract-treated psoriasis-like dermatitis-induced mice lead to the conclusion that the combination extract from all the plants was instrumental in downregulating the overexpressed cytokines, which was followed by the CL extract. Moreover, lesser yet positive response was evident from CP and TC extracts. The results suggest that these plants can prove to have tremendous preventive potential against the disease and can open the way to new therapeutic strategies for psoriasis treatment.

Topics: Aloe; Aminoquinolines; Animals; Celastrus; Curcuma; Cytokines; Dermatitis, Contact; Drug Evaluation, Preclinical; Gene Expression; Imiquimod; Male; Mice; Plant Extracts; Plant Stems; Plants, Medicinal; Psoriasis; Skin; Tinospora

Topics: Curcumin; Dermatitis, Contact; Extracellular Matrix; Fibroblasts; Humans; Keloid; Quercetin

Nickel can induce cellular and nuclear damages responsible for chronic diseases, like allergic contact dermatitis (ACD). We previously showed that matrix metalloproteinase-2 (MMP-2) gene expression was induced by nickel in nontumorigenic human keratinocytes cell line (HaCat).. To investigate the signal transduction pathways involved in gelatinolytic activity induced in HaCat under nickel stimulation.. We analyzed the involvement of protein kinase A (PKA), protein kinase C (PKC), tyrosine kinase (PTK), nuclear factor-kB (NF-kB) and activator protein-1 (AP-1) using specific inhibitors (H89, calphostin C, genistein, carpain and curcumin) by electrophoretic mobility shift assay, reverse transcription-polymerase chain reaction and gelatin zymography.. Our results indicate that nickel-induced MMP-2 production was inhibited with PTK, PKC and AP-1 specific inhibitors. Moreover, both PKA and NF-kB were not involved in nickel pathway.. Using HaCat, we showed that curcumin and genistein can revert nickel-induced MMP-2 upregulation. Whether the use of PTK and AP-1 inhibitors has therapeutic ramifications in the management of ACD remains to be investigated.

Topics: Cell Line, Transformed; Curcumin; Dermatitis, Contact; Drug Combinations; Enzyme Inhibitors; Gene Expression Regulation; Genistein; Humans; Irritants; Keratinocytes; Matrix Metalloproteinase 2; Matrix Metalloproteinase Inhibitors; Nickel; Protein-Tyrosine Kinases; RNA, Messenger; Signal Transduction; Tissue Inhibitor of Metalloproteinase-1; Tissue Inhibitor of Metalloproteinase-2; Transcription Factor AP-1; Up-Regulation

Topical application of curcumin, the yellow pigment in turmeric and curry, strongly inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ornithine decarboxylase activity, DNA synthesis, and tumor promotion in mouse skin (Huang et al., Cancer Res., 48: 5941-5946, 1988). Chlorogenic acid, caffeic acid, and ferulic acid (structurally related dietary compounds) were considerably less active. In the present study, topical application of curcumin markedly inhibited TPA- and arachidonic acid-induced epidermal inflammation (ear edema) in mice, but chlorogenic acid, caffeic acid, and ferulic acid were only weakly active or inactive. The in vitro addition of 3, 10, 30, or 100 microM curcumin to cytosol from homogenates of mouse epidermis inhibited the metabolism of arachidonic acid to 5-hydroxyeicosatetraenoic acid (5-HETE) by 40, 60, 66, or 83%, respectively, and the metabolism of arachidonic acid to 8-HETE was inhibited by 40, 51, 77, or 85%, respectively [IC50 (concentration needed for 50% inhibition) = 5-10 microM]. Chlorogenic acid, caffeic acid, or ferulic acid (100 microM) inhibited the metabolism of arachidonic acid to 5-HETE by 36, 10, or 16%, respectively, and these hydroxylated cinnamic acid derivatives inhibited the metabolism of arachidonic acid to 8-HETE by 37, 20, or 10%, respectively (IC50 greater than 100 microM). The metabolism of arachidonic acid to prostaglandin E2, prostaglandin F2 alpha, and prostaglandin D2 by epidermal microsomes was inhibited approximately 50% by the in vitro addition of 5-10 microM curcumin. Chlorogenic acid, caffeic acid, and ferulic acid (100 microM) were inactive. In vitro rat brain protein kinase C activity was not affected by 50-200 microM curcumin, chlorogenic acid, caffeic acid, or ferulic acid. The inhibitory effects of curcumin, chlorogenic acid, caffeic acid, and ferulic acid on TPA-induced tumor promotion in mouse epidermis parallel their inhibitory effects on TPA-induced epidermal inflammation and epidermal lipoxygenase and cyclooxygenase activities.

Topics: Animals; Arachidonic Acid; Arachidonic Acids; Caffeic Acids; Chlorogenic Acid; Coumaric Acids; Curcumin; Dermatitis, Contact; Female; Hydroxyeicosatetraenoic Acids; In Vitro Techniques; Lipoxygenase; Mice; Peroxidases; Prostaglandin-Endoperoxide Synthases; Tetradecanoylphorbol Acetate

Topics: Curcuma; Dermatitis, Contact; Dermatitis, Occupational; Humans; Male; Middle Aged; Patch Tests; Plant Extracts