The massive production and activation of myofibroblasts (MFB) is key to the development of liver fibrosis. In many studies, it has been proven that hepatocytes are an important part of MFB, and can be transformed into MFB through epithelial-mesenchymal transition (EMT) during hepatic fibrogenesis. In our previous study, we confirmed that curcumin inhibited EMT procession and differentiation of hepatocytes into MFB. In addition, in previous studies, it has been shown that autophagy plays an important role in the regulation of cellular EMT procession. In the current study, we showed that curcumin inhibited TGF-β/Smad signaling transmission by activating autophagy, thereby inhibiting EMT. The mechanism of degradative polyubiquitylation of Smad2 and Smad3 is likely through inhibiting tetratricopeptide repeat domain 3 (TTC3) and by inducing ubiquitylation and proteasomal degradation of Smad ubiquitination regulatory factor 2 (SMURF2), which on account of the increase of autophagy in hepatocytes. Curcumin inhibits levels of reactive oxygen species (ROS) and oxidative stress in hepatocytes by activating PPAR-α, and regulates upstream signaling pathways of autophagy AMPK and PI3K/AKT/mTOR, leading to an increase of the autophagic flow in hepatocytes. In this study, we confirm that curcumin effectively reduced the occurrence of EMT in hepatocytes and inhibited production of the extracellular matrix (ECM) by activating autophagy, which provides a potential novel therapeutic strategy for hepatic fibrosis.

Sulforaphane, a naturally occurring compound found in cruciferous vegetables, has been shown to be neuroprotective in several neurological disorders. In this study, we sought to investigate the potential protective effects and associated molecular mechanisms of sulforaphane in an in vivo Parkinson’s disease (PD) model, based on rotenone-mediated neurotoxicity. Our results showed that sulforaphane inhibited rotenone-induced locomotor activity deficiency and dopaminergic neuronal loss. Additionally, sulforaphane treatment inhibited the rotenone-induced reactive oxygen species production, malondialdehyde (MDA) accumulation and resulted in an increased level of total glutathione and reduced glutathione (GSH): oxidized glutathione (GSSG) in the brain. Western blot analysis illustrated that sulforaphane increased the expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2), heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase (NQO1), the latter two of which are anti-oxidative enzymes. Moreover, sulforaphane treatment significantly attenuated rotenone-inhibited mTOR-mediated p70S6K and 4E-BP1 signalling pathway, as well as neuronal apoptosis. In addition, sulforaphane rescued rotenone-inhibited autophagy, as detected by LC3-II. Collectively, these findings demonstrated that sulforaphane exert neuroprotective effect involving Nrf2-dependent reductions in oxidative stress, mTOR-dependent inhibition of neuronal apoptosis and the restoration of normal autophagy. Sulforaphane appears to be a promising compound with neuroprotective properties that may play an important role in preventing PD.

Gut microbiota drives the attenuation of dextran sulphate sodium-induced colitis by Huangqin decoction Gut microbiota drives the attenuation of dextran sulphate sodium-induced colitis by Huangqin decoction

Nuclear factor-erythroid 2-related factor 2 (Nrf2) has emerged as a novel target for the prevention of colorectal cancer (CRC). Many chemopreventive compounds associated with Nrf2 activation are effective in preclinical systems and many on-going clinical trials are showing promising findings. In present study we evaluated the cytoprotective effect and chemopreventive properties of dietary digitoflavone.