Physiological and Metabolomic Alterations in Macrocystis pyrifera upon Exposure to Chromium(VI)

1593-1599In order to comprehensively characterize the effects of chromium (VI) on physiological and metabonomic performance of Macrocystis pyrifera, the sporophytes were exposed to 2 mg L-1 potassium dichromate for 3 days. M. pyrifera sporophytes showed decreased pigment content and Chla fuloresecnece parameters with the accumulation of Cr(VI). The carbon content was clearly increased, while the content of nitrogen, hydrogen and sulfur were little changed. Moreover, an untargeted metabolomic analysis was carried out in order to investigate the metabolic effects and to obtain a comprehensive profiling of induced metabolites during Cr stress. Absolute quantification of 14 different metabolites was obtained through GC-MS methods. The principal component analysis showed a clear separation between control and Cr treated samples. Some pathways including carbon fixation, sulfur metabolism, taurine and hypotaurine metabolism were affected by Cr (VI) stress. These findings provided valuable information to elucidate the mechanism of M. pyrifera upon Cr (VI) stress

Arctigenin alleviates ER stress via activating AMPK

Aim: To investigate the protective effects of arctigenin (ATG), a phenylpropanoid dibenzylbutyrolactone lignan from Arctium lappa L (Compositae), against ER stress in vitro and the underlying mechanisms. Methods: A cell-based screening assay for ER stress regulators was established. Cell viability was measured using MTT assay. PCR and Western blotting were used to analyze gene and protein expression. Silencing of the CaMKKβ, LKB1, and AMPKα1 genes was achieved by RNA interference (RNAi). An ATP bioluminescent assay kit was employed to measure the intracellular ATP levels. Results: ATG (2.5, 5 and 10 μmol/L) inhibited cell death and unfolded protein response (UPR) in a concentration-dependent manner in cells treated with the ER stress inducer brefeldin A (100 nmol/L). ATG (1, 5 and 10 μmol/L) significantly attenuated protein synthesis in cells through inhibiting mTOR-p70S6K signaling and eEF2 activity, which were partially reversed by silencing AMPKα1 with RNAi. ATG (1-50 μmol/L) reduced intracellular ATP level and activated AMPK through inhibiting complex I-mediated respiration. Pretreatment of cells with the AMPK inhibitor compound C (25 μmol/L) rescued the inhibitory effects of ATG on ER stress. Furthermore, ATG (2.5 and 5 μmol/L) efficiently activated AMPK and reduced the ER stress and cell death induced by palmitate (2 mmol/L) in INS-1 β cells. Conclusion: ATG is an effective ER stress alleviator, which protects cells against ER stress through activating AMPK, thus attenuating protein translation and reducing ER load