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Gastric cancer (GC) is one of the most malignant tumors with high incidence and mortality worldwide, and the multidrug resistance (MDR) often results in chemotherapy failure in GC. DJ-1 has been well indicated to be associated with drug resistance in multiple cancers. However, the role of DJ-1 in the MDR of gastric cancer cells and its possible mechanism remain to be elucidated. Therefore, the current study was investigated whether DJ-1 expression is differential in parental gastric cancer cell SGC7901 and vincristine (VCR)-induced gastric cancer MDR cell SGC7901/VCR, and whether DJ-1 plays a significant role in development of MDR in gastric cancer. The results showed that DJ-1 expression in SGC7901/VCR cells was significantly higher than its sensitive parental SGC7901 cells. Furthermore, DJ-1 overexpressed gastric cancer cell line SGC7901/LV-DJ-1 led to the increase of cell survival rate, the IC 50 of chemotherapeutic drugs and number of cell clones as well as decrease of cell cycle G0/G1 phase ratio compared with its parental cells under the treatment of VCR, adriamycin (ADR), 5-Fluorouracil (5-FU) and cisplatin (DDP). However, the DJ-1 knockdown stable cell line SGC7901/VCR/shDJ-1 reversed the above mentioned series of MDR. Moreover, it was found that upregulation of DJ-1 protein expression promoted the pumping rate of GC cells to ADR and reduced the apoptotic index of GC cells treated with chemotherapeutic drugs by upregulating P-gp and Bcl-2. Similarly, knocking down DJ-1, P-gp or Bcl-2 displayed a converse effect. In conclusion, the current study demonstrated that DJ-1 overexpression confers the MDR phenotype to SGC7901 cells and this process is related to DJ-1 promoting active efflux of drugs and enhancing the anti-apoptotic ability of MDR GC cells by upregulating P-gp and Bcl-2. • DJ-1 expression in SGC7901/VCR cells was significantly higher than SGC7901 cells. • SGC7901/VCR and SGC7901/LV-DJ-1 cells led to a series of MDR phenomenon. • DJ-1 overexpression promoted the adriamycin pumping rate of SGC7901 cells. • DJ-1 overexpression reduced the apoptotic index of SGC7901 cells. • DJ-1 overexpression upregulated P-gp and Bcl-2 expression of SGC7901 cells. [ABSTRACT FROM AUTHOR]

• Develop micro-kinetic models of electrocatalytic PCET reactions. • Propose theory for optimizing catalysts and reaction conditions for PCET. • Validate the theory by experiment on model catalysts for CO 2 reduction. Understanding the effects of pH and potential on proton-coupled electron transfer (PCET) steps and optimizing the reaction activity are of key importance for efficient applications of energy conversion processes. In this work, we develop a simple theory to optimize the electrocatalytic PCET reactions, in which electron and proton transfer take place in sequential steps, by combining an energy level diagram and micro-kinetic theories. Our theory suggests matching conditions on PCET energetics (redox potentials and p K a 's) and reaction environments (potential and pH) in order to achieve maximum kinetics. Consequently, a descriptor representing deviation from the ideal condition, i.e. |Δ U re |+ 2.30 k B T/ e |Δp K a |, is proposed to measure catalyst (in)activity. To test our theory, we further investigate CO 2 electroreduction on a model catalyst both computationally and experimentally, and show that the activity for CO 2 reduction on FePc (Iron Phthalocyanine) molecule is higher than H 2 evolution at near neutral condition. Our theory not only identifies the individual contribution of electron and proton transfer to overpotentials but also provides simple guidelines for optimizing the experimental conditions and searching for efficient catalysts. [ABSTRACT FROM AUTHOR]

Resveratrol, a multi-functional phytoalexin, has been well indicated to exert cardioprotective effects by weakening ischemia/reperfusion (I/R) injury, and cell apoptosis is a vital way in I/R injury. SIRT1-p53 pathway has strong significance in regulating cell apoptosis. DJ-1 can directly bind to SIRT1 and stimulate the activity of SIRT1-p53. Therefore, the current study was determined whether Resveratrol attenuates hypoxia/reoxygenation (H/R)-induced cell apoptosis, and whether DJ-1-mediated SIRT1 activation involves in the cardioprotective effects of Resveratrol. The results showed that remarkable decrease in the number of apoptotic cells along with reduction of lactate dehydrogenase release and restoration of cell viability emerged when Resveratrol was applied in the H9c2 cells exposed to H/R. Moreover, Resveratrol increased DJ-1 expression and promoted the interaction of DJ-1 with SIRT1, which further contributed to subsequent restoration of SIRT1 activity and decrease of acetylation level of p53. However, above cardioprotective effects of Resveratrol were abrogated by DJ-1 siRNA and SIRT1 specific inhibitor Sirtinol. In conclusion, the current study demonstrated that Resveratrol suppressed H/R-induced cell apoptosis, which may be conducted by up-regulating DJ-1, and later activating SIRT1 activity and subsequently inhibiting p53 acetylation level in the H9c2 cells. • Resveratrol increased the DJ-1 expression and promoted the interaction of DJ-1 with SIRT1 in the H9c2 cells exposed to H/R. • Resveratrol restored SIRT1 activity in a way of DJ-1-dependence in the H9c2 cells exposed to H/R. • Resveratrol decreased H/R-induced p53 acetylation level by DJ-1-mediated SIRT1 activation in the H9c2 cells. • Resveratrol attenuated H/R-induced cell apoptosis by DJ-1-mediated SIRT1 activation in the H9c2 cells. [ABSTRACT FROM AUTHOR]