Sahdev Anil K, Raj Vinit, Singh Ashok K, Rai Amit, Keshari Amit K, De Arnab, Samanta Amalesh, Kumar Umesh, Rawat Atul, Kumar Dinesh, Nath Sneha, Prakash Anand, Saha Sudipta
a Department of Pharmaceutical Sciences , Babasaheb Bhimrao Ambedkar University , Vidya Vihar, Lucknow , India.
b Department of Pharmaceutical Technology , Jadavpur University , Kolkata , West Bengal , India.
Cancer Biol Ther. 2017 May 4;18(5):304-313. doi: 10.1080/15384047.2017.1310341. Epub 2017 Mar 30.
Pyrazinoic acid (PA) is structurally similar to nicotinic acid which acts on G-protein-coupled receptor (GPR109A). GPR109A expresses in colonic and intestinal epithelial sites, and involves in DNA methylation and cellular apoptosis. Therefore, it may be assumed that PA has similar action like nicotinic acid and may be effective against colorectal carcinoma (CRC). CRC was produced via subcutaneous injection of dimethylhydrazine (DMH) at 40 mg/kg body weight once in a week for 4 weeks. After that, PA was administered orally at 2 doses of 10 and 25 mg/kg daily for 15 d to observe the antiproliferative effect. Various physiologic, oxidative stress, molecular parameters, histopathology, RT-PCR and NMR based metabolomics were performed to evaluate the antiproliferative potential of PA. Our results collectively suggested that PA reduced body weight, tumor volume and incidence no. to normal. It restored various oxidative stress parameters and normalized IL-2, IL-6, and COX-2 as compared with carcinogen control. In molecular level, overexpressed IL-6 and COX-2 genes became normal after PA administration. Again, normal tissue architecture was prominent after PA administration. Score plots of PLS-DA models exhibited that PA treated groups were significantly different from CRC group. We found that CRC rat sera have increased levels of acetate, glutamine, o-acetyl-glycoprotein, succinate, citrulline, choline, o-acetyl choline, tryptophan, glycerol, creatinine, lactate, citrate and decreased levels of 3-hydroxy butyrate, dimethyl amine, glucose, maltose, myoinositol. Further the PA therapy has ameliorated the CRC-induced metabolic alterations, signifying its antiproliferative properties. In conclusion, our study provided the evidence that PA demonstrated good antiproliferative effect on DMH induced CRC and thus demonstrated the potential of PA as a useful drug for future anticancer therapy.
吡嗪酸(PA)在结构上与作用于G蛋白偶联受体(GPR109A)的烟酸相似。GPR109A在结肠和肠道上皮部位表达,并参与DNA甲基化和细胞凋亡。因此,可以推测PA具有与烟酸相似的作用,可能对结直肠癌(CRC)有效。通过每周一次皮下注射40mg/kg体重的二甲基肼(DMH),持续4周来诱导产生CRC。之后,每天以10和25mg/kg两种剂量口服PA,持续15天,以观察其抗增殖作用。进行了各种生理、氧化应激、分子参数、组织病理学、基于RT-PCR和核磁共振的代谢组学研究,以评估PA的抗增殖潜力。我们的结果共同表明,PA使体重、肿瘤体积和发病率降低至正常水平。与致癌物对照组相比,它恢复了各种氧化应激参数,并使白细胞介素-2(IL-2)、白细胞介素-6(IL-6)和环氧化酶-2(COX-2)水平正常化。在分子水平上,PA给药后,过表达的IL-6和COX-2基因恢复正常。此外,PA给药后正常的组织结构明显。偏最小二乘判别分析(PLS-DA)模型的得分图显示,PA治疗组与CRC组有显著差异。我们发现,CRC大鼠血清中乙酸盐、谷氨酰胺、O-乙酰糖蛋白、琥珀酸盐、瓜氨酸、胆碱、O-乙酰胆碱、色氨酸、甘油、肌酐、乳酸、柠檬酸盐水平升高,而3-羟基丁酸盐、二甲胺、葡萄糖、麦芽糖、肌醇水平降低。此外,PA治疗改善了CRC诱导的代谢改变,表明其具有抗增殖特性。总之,我们的研究提供了证据,表明PA对DMH诱导的CRC具有良好的抗增殖作用,从而证明了PA作为未来抗癌治疗有用药物的潜力。