Aqueous and polyphenol-rich Larrea divaricata Cav. extracts as potential skin care agents

Skin cells are affected by UV-induced oxidative stress resulting in photoaging and diseases. The objective of this work was to assess the effect of an aqueous extract of Larrea divaricata(Aq) and a flavonoid rich fraction (EA), obtained by liquid/liquid fractionation, on the proliferation of keratinocytes and fibroblasts by the tritiated thymidine uptake assay and on cell viability by the trypan blue exclusion assay. The in vitro sun protection factor (SPF), peroxidase (Px)-like and superoxide dismutase (SOD)-like activities were determined by kinetic spectrophotometric assays, and the phytochemical composition was determined by HPLC-UV and HPLC MS/MS.Aq and EA induced keratinocytes and fibroblast proliferation, protected fibroblasts from H2O2-induced apoptosis and exerted SOD-like and Px-like activities. Aq and EA had a high sun UVB protection factor. So, L. divaricatacould be used in a future for the development of new dermocosmetic or phytotherapy adjuvant in skin oxidative damage.

Vandellia Cordifolia Regulated Cell Proliferation and Cytokines Production in Human Mononuclear Cells

Vandellia cordifolia (V. cordifolia) used for treatment inflammation in traditional Chinese medicine was selected for immunopharmacological activity test. The effects of V. cordifolia extracted fractions on human mononuclear cells (HMNC) proliferation were determined by tritiated thymidine uptake. The results indicated that VC-ME fraction suppressed HMNC proliferation activated with phytohemagglutinin (PHA) and stimulated cell cycle progression was arrested at the G0/G1 stage. The inhibitory mechanisms may involve the blocking of interleukin-2 (IL-2) and interferon-γ (IFN-γ) production, since VC-ME suppressed IL-2 and IFN-γ production of HMNC in a dose-dependent manner. Therefore, it is suggested that immunomodulatory agents are contained in V. cordifolia.

Regulation of macrophage growth responses to colony-stimulating factor-1 by 1,25-dihydroxyvitamin D3.

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) has previously been shown to affect the biology of a variety of immune cells, including the functions of macrophages. The effect of the vitamin D metabolite on the proliferative responses of macrophages to the cytokine colony-stimulating factor-1 (CSF-1) has been studied. It was found that this substance was able to suppress the growth responses of macrophages to CSF-1 as assessed by macrophage-tritiated thymidine uptake and also by cell counts. The effect was specific to this vitamin D metabolite because another vitamin D analogue, 25 hydroxyvitamin D3, did not have a similar effect on the responses of such cells to CSF-1. The results yield information on the regulatory role of 1,25(OH)2D3 on macrophage growth. It would appear that this vitamin D metabolite may act as a negative autoregulatory cytokine because it is produced by the macrophage when it is activated. A schema can be envisaged where CSF-1 is delivered to the macrophage to activate it and to cause it to proliferate. In the process, it also secretes 1,25(OH)2D3, which exerts a suppressive action to dampen this response.

Caco-2 cells express type I interleukin-1 receptors: ligand binding enhances proliferation

We examined the effect of interleukin-1 (IL-1) on the rate of proliferation of the human colon carcinoma Caco-2 and characterized the human intestinal epithelial cell IL-1 receptor (IL-1R). IL-1 dose dependently increased tritiated thymidine uptake in confluent Caco-2 monolayers fed complete growth medium. An anti-IL-1 beta completely blocked the increase in tritiated thymidine uptake, whereas an IL-1 receptor antagonist human recombinant blocked it partially. In long-term culture, IL-1 increased DNA content over control, an effect similar to that of epidermal growth factor (EGF). Unlike EGF, IL-1 did not enhance tritiated thymidine uptake in Caco-2 monolayers grown in serum-free medium, implying that IL-1 needs a cofactor(s) to elicit its proliferative effect. Cross-linking 125I-IL-1 beta to Caco-2 membranes revealed a binding protein of approximately 80 kDa with binding saturated at approximately 2.5 x 10(9) M-1 consistent with that for the type I IL-1R. cDNA transcribed from Caco-2 mRNA and amplified by polymerase chain reaction, using complementary oligonucleotides, resulted in a reaction product matching the sequence of the type I IL-1R. Our results demonstrate that IL-1 enhances proliferation of Caco-2 cells. This effect requires the presence of an unidentified cofactor(s). Also, Caco-2 cells express the type I IL-1R.