Selected article for: "concentration dependent manner and TNF Î"
Author: Manandhar, Bandana; Paudel, Pradeep; Seong, Su Hui; Jung, Hyun Ah; Choi, Jae Sue
Title: Characterizing Eckol as a Therapeutic Aid: A Systematic Review
  • Document date: 2019_6_18
    • ID: 0dpv85od_176
    Snippet: In acne vulgaris, P. acnes bacteria [143] stimulates keratinocytes to activate TNF-α and ILs and other inflammatory mediators including nitric oxide secretion [144] . With an increase in MMPs, there is degradation of collagen in dermis infected with acne, which is predicted to form degraded/disintegrated collagen in the tissue [43] . The P. acnes-induced inflammatory response in HaCaT cells is due to MMP-2 and MMP-9 [145] . Eckol (1, 5, and 10 Â.....
    Document: In acne vulgaris, P. acnes bacteria [143] stimulates keratinocytes to activate TNF-α and ILs and other inflammatory mediators including nitric oxide secretion [144] . With an increase in MMPs, there is degradation of collagen in dermis infected with acne, which is predicted to form degraded/disintegrated collagen in the tissue [43] . The P. acnes-induced inflammatory response in HaCaT cells is due to MMP-2 and MMP-9 [145] . Eckol (1, 5, and 10 µM) slightly decreased the MMP-2 and MMP−9 mRNA levels. Also, P. acnes activated the NF-κB pathway, which is related to inflammatory mediators TNF-α, iNOS, and COX-2, and also the phosphorylation of p65 (an activated NF-κB subunit). Eckol gradually decreased all those activations in a concentration-dependent manner. Whereas treatment with P. acnes accelerated the phosphorylation of Akt which was inhibited by eckol in HaCaT cells [71] .

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