1.Eicosapentaenoic and docosahexaenoic acids-rich fish oil supplementation attenuates strength loss and limited joint range of motion after eccentric contractions: a randomized, double-blind, placebo-controlled, parallel-group trial.
Tsuchiya Y1, Yanagimoto K2, Nakazato K3, Hayamizu K4, Ochi E5. Eur J Appl Physiol. 2016 Apr 16. [Epub ahead of print]
PURPOSE: This study investigated the effect of eicosapentaenoic and docosahexaenoic acids-rich fish oil (EPA + DHA) supplementation on eccentric contraction-induced muscle damage.
2.Non-enzymatic electrochemical biosensor based on Pt NPs/RGO-CS-Fc nano-hybrids for the detection of hydrogen peroxide in living cells.
Bai Z1, Li G2, Liang J1, Su J3, Zhang Y4, Chen H4, Huang Y5, Sui W6, Zhao Y7. Biosens Bioelectron. 2016 Apr 8;82:185-194. doi: 10.1016/j.bios.2016.04.004. [Epub ahead of print]
A highly sensitive non-enzymatic electrochemical sensor based on platinum nanoparticles/reduced graphene oxide-chitosan-ferrocene carboxylic acid nano-hybrids (Pt NPs/RGO-CS-Fc biosensor) was developed for the measurement of hydrogen peroxide (H2O2). The RGO-CS-Fc nano-hybrids was prepared and characterized by UV-vis spectrum, Fourier transform infrared spectroscopy, transmission electron microscopy, Raman spectrometer and electrochemical impedance spectroscopy. Under optimal experimental conditions, the Pt NPs/RGO-CS-Fc biosensor showed outstanding catalytic activity toward H2O2 reduction. The current response of the biosensor presented a linear relationship with H2O2 concentration from 2.0×10-8M to 3.0×10-6M with a correlation coefficient of R2=0.9968 and with logarithm of H2O2 concentration from 6.0×10-6M to 1.0×10-2M with a correlation coefficient of R2=0.9887, the low detection limit of 20nM was obtained at the signal/noise (S/N) ratio of 3.
3.Crosstalk between liver antioxidant and the endocannabinoid systems after chronic administration of the FAAH inhibitor, URB597, to hypertensive rats.
Biernacki M1, Łuczaj W1, Gęgotek A1, Toczek M2, Bielawska K1, Skrzydlewska E3. Toxicol Appl Pharmacol. 2016 Apr 13. pii: S0041-008X(16)30076-X. doi: 10.1016/j.taap.2016.04.006. [Epub ahead of print]
Hypertension is accompanied by perturbations to the endocannabinoid and antioxidant systems. Thus, potential pharmacological treatments for hypertension should be examined as modulators of these two metabolic systems. The aim of this study was to evaluate the effects of chronic administration of the fatty acid amide hydrolase (FAAH) inhibitor [3-(3-carbamoylphenyl)phenyl]N-cyclohexylcarbamate (URB597) on the endocannabinoid system and on the redox balance in the livers of DOCA-salt hypertensive rats. Hypertension caused an increase in the levels of endocannabinoids [anandamide (AEA), 2-arachidonoyl-glycerol (2-AG) and N-arachidonoyl-dopamine (NADA)] and CB1 receptor and the activities of FAAH and monoacylglycerol lipase (MAGL). These effects were accompanied by an increase in the level of reactive oxygen species (ROS), a decrease in antioxidant activity/level, enhanced expression of transcription factor Nrf2 and changes to Nrf2 activators and inhibitors.
4.Deoxycholic acid mediates non-canonical EGFR-MAPK activation through the induction of calcium signaling in colon cancer cells.
Centuori SM1, Gomes CJ2, Trujillo J2, Borg J1, Brownlee J1, Putnam CW3, Martinez JD4. Biochim Biophys Acta. 2016 Apr 13. pii: S1388-1981(16)30100-7. doi: 10.1016/j.bbalip.2016.04.006. [Epub ahead of print]
Obesity and a western diet have been linked to high levels of bile acids and the development of colon cancer. Specifically, increased levels of the bile acid deoxycholic acid (DCA), an established tumor promoter, has been shown to correlate with increased development of colorectal adenomas and progression to carcinoma. Herein we investigate the mechanism by which DCA leads to EGFR-MAPK activation, a candidate mechanism by which DCA may promote colorectal tumorigenesis. DCA treated colon cancer cells exhibited strong and prolonged activation of ERK1/2 when compared to EGF treatment alone. We also showed that DCA treatment prevents EGFR degradation as opposed to the canonical EGFR recycling observed with EGF treatment. Moreover, the combination of DCA and EGF treatment displayed synergistic activity, suggesting DCA activates MAPK signaling in a non-canonical manner. Further evaluation showed that DCA treatment increased intracellular calcium levels and CAMKII phosphorylation, and that blocking calcium with BAPTA-AM abrogated MAPK activation induced by DCA, but not by EGF.