Salicin is a natural COX inhibitor.
Significant down regulation of PGE2, the enzymatic product of COX2, to 76% in lysate and 70% in supernatant is observed with Salicin 10 μM treatment in COLO cells when compare to the COLO control. This is accompanied with a minimal COX1 inhibition to 91% of the CCD control on the genetic level. Treatment with Salicin 1 μM decreases colon cancer cell proliferation rates from 144% to 113% at 24 hours and 187% to 130% at 48 hours, with 10 μM decreasing proliferation rates to108% at 24 hours and 119% at 48 hours[1]. The concentrations of TNF-α, IL-1β and IL-6 of LPS-induced cells pretreated with 0.07, 0.14 and 0.28 μM Salicin are significant reduced compare with LPS group[2].
Salicin (D(-)-Salicin) (35, 70, 140 μM) markedly inhibits the LPS-induced pathological changes. MPO activity in LPS-induced lung tissue is significantly increased compare with control group. However, Salicin (35, 70, 140 μM) markedly inhibits this change. Pretreatment with Salicin inhibits LPS-induced activation of JNK, ERK, p38/MAPK and p65 in a dose-dependent manner[2].
References:
[1]. Jun Yan He, et al. Salicin as a Multipurpose Therapeutic Approach for Colon Cancer.
[2]. Li Y, et al. D(-)-Salicin inhibits the LPS-induced inflammation in RAW264.7 cells and mouse models. Int Immunopharmacol. 2015 Jun;26(2):286-94.