Effect of Baricitinib on TPA-induced psoriasis like skin inflammation.

Psoriasis is a chronic inflammatory disorder of the skin and is characterized by hyper-dividing keratinocytes. This hyper-proliferation of keratinocytes is due to the high level of inflammatory cytokines. In this study, we evaluated the effect of topically applied Baricitinib, JAK1/2 inhibitor on chronic 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced psoriasis model in mice. To our knowledge, this is the first report evaluating the topical route of administration of Baricitinib in the context of psoriasis in vivo. TPA-induced inflammation was induced by the topical application of TPA in both ears. Thirty minutes before the application of TPA, the inner and outer surface of each ear was treated with Baricitinib for 6 days. Topical application of Baricitinib inhibited the expression of inflammation markers up-regulated by TPA. Besides, Baricitinib substantially reduced ear swelling, infiltration of leukocytes, the proliferation of epidermal cells, and angiogenesis of the dermal layer. The results suggest that Baricitinib significantly reduced phosphorylation of STAT3 and STAT1 levels in turn attenuating the downstream expression of inflammatory cytokines. Collectively, these results suggest that Baricitinib can be a potential therapeutic through topical route for psoriasis progresses.

Hepatoprotective and antioxidant activity of standardized herbal extracts.

BACKGROUND: Phyllanthus emblica, Camellia sinensis, Mangifera indica, Punica granatum, and Acacia catechu have been shown to possess widespread pharmacological application against multitude of diseases namely cancer, diabetes, liver disorders, and oxidative stress. OBJECTIVE: We evaluated the hepatoprotective activity of the standardized herbal extracts against tert-butyl hydroperoxide (t-BH) induced toxicity and their mechanism of hepatoprotective action in human hepatocarcinoma cells (HepG2 cell line). MATERIALS AND METHODS: The hepatoprotective activity was studied by observing the effect of these herbal extracts on t-BH induced reduction in cell viability of HepG2 cells. In addition, the reducing power of the extracts and their ability to scavenge free radicals were evaluated using two antioxidant assay systems: cell free [oxygen radical absorbance capacity (ORAC), 2,2-diphenyl-1-picrylhydrazyl (DPPH), and [2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonicacid)] (ABTS)] and cell based [cellular antioxidant activity (CAA)]. RESULTS AND DISCUSSION: The results obtained showed that these extracts possess significant hepatoprotective activity. This may indicate that the plant extracts contain compounds, which can remove toxic metabolites following t-BH induced toxicity. The extracts exhibited significant antioxidant property as evident by the Trolox values and effective scavenging of DPPH and ABTS radicals. The extracts also demonstrated inhibition of AAPH-induced fluorescence in HepG2 cells. These results indicate the ability of the plant extracts to protect the liver cells from chemical-induced damage, which might be correlated to their radical scavenging potential. CONCLUSION: This study demonstrates that these extracts have potential hepatoprotective activity which is mainly attributed to the antioxidant potential, which might occur by reduction of lipid peroxidation and cellular damage.