Curcumin has been demonstrated to affect the chemoresistance in cancer cells of various origins. However, its ability to modulate lactate-induced chemoresistance remains unclear. The Present investigation demonstrates that curcumin inhibits the survival of HepG2 and HuT78 cells and can modulate chemo-susceptibility of HepG2 cells. Experimental simulation of simultaneous and pre-treatment suggest cooperatively between curcumin and anticancer drugs as well as the modulation of molecular regulators. Inhibition of glucose consumption, lactate production, extracellular acidity and augmented level of Nitric oxide were observed. DAPI staining revealed hyper condensation of chromatin in curcumin-treated HepG2 cells. Curcumin also diminished the lactate-induced chemoresistance against doxorubicin in hepatic cancer cells along with down regulation of lactate receptor (hydroxycarboxylic acid receptor-1; HCAR-1/GPR81). Alteration of the extracellular milieu along with inhibited expression of genes (hif-1α, ldh-a, mct-1, mdr-1 and stat-3) and proteins (HIF-1α and HCAR-1) are indicated to be involved in curcumin-induced reversal of chemoresistance in HepG2 cells. Findings of present investigation contribute to knowledge of curcumin mediated chemosensitization and its mechanism.

姜黄素已被证明可影响多种来源的癌细胞的化学耐药性。然而，其调节乳酸盐诱导的化学抗性的能力仍不清楚。本研究表明姜黄素抑制HepG2和HuT78细胞的存活，并可以调节HepG2细胞的化学敏感性。同时和预处理的实验模拟表明姜黄素和抗癌药之间的协同作用以及分子调节剂的调节作用。观察到抑制葡萄糖消耗，乳酸产生，细胞外酸性和一氧化氮水平升高。DAPI染色显示在姜黄素处理的HepG2细胞中染色质高度浓缩。ħ ydroxy Ç arboxylic一个CID ř eceptor-1; HCAR-1 / GPR81）。姜黄素与细胞外环境的改变以及基因（hif-1α，ldh-a，mct-1，mdr-1和stat-3）和蛋白质（HIF-1α和HCAR-1）的表达受抑制有关诱导的HepG2细胞化学耐药性逆转。本研究的发现有助于了解姜黄素介导的化学致敏作用及其机理。