In vitro effect of glycoglycochenodeoxycholic acid on viability and reactive oxygen species in Echinococcus granulosus protoscoleces
TANG Guang-yao1, JIANG Yu-feng1, LYU Hai-long2, LI Jia-jie4, YANG Ren-tan5, QIN Wen-juan6, MA Bin3, MA Rong-ji4, WANG Lin-yao1, CHEN Lin4, XU Ya4
1.Department of Basic Medicine, Chengdu Medical College, Chengdu 610000, China; 2.Department of Hepatobiliary Surgery, The third people’s hospltal of chengdu, Chengdu 610000, China; 3.Department of Hepatobiliary Surgery, The First Affiliated Hospital, School of Medicine, Shihezi University, Shihezi 832008, China; 4.Department of Histology and Embryology, School of Medicine, Shihezi University, Shihezi 832008, China; 5.The First People’s Hospital of Jining City, Jining 272000, China; 6. Department of Ultrasound Diagnosis, the First Affiliated Hospital, School of Medicine, Shihezi University, Shihezi 832008, China
Abstract:The aim of this study is to investigate the in vitro effect of glycochenodeoxycholic acid (GCDCA) on viability and reactive oxygen species in Echinococcus granulosus protoscoleces. After incubated several days, E.granulosus protoscoleces were randomly allocated into five groups: untreated group, DMSO group, 500 μmol/L group, 1 500 μmol/L group, 2 500 μmol/L group.The effect of GCDCA on protoscoleces viability was investigated using 0.1% eosin staining. Reactive oxygen species (ROS detection kit) was used to detect ROS and Caspase-3 activity was measured using a caspase-3 activity assay kit. Results showed that different concentrations of GCDCA can inhibit protoscoleces' viability, and with prolongation of the time of GCDCA action and increase of its concentration, the inhibitory effect on protoscoleces is gradually increased. In addition, GCDCA increased the mortality of protoscoleces in a concentration-dependent. During the incubation time, the production of ROS and caspase-3 activity clearly increased in protoscoleces treated with GCDCA for 24 hours compared with that in controls (P<0.05). At last, We founded that GCDCA had an inhibitory effect on the growth of E. granulosus protoscoleces, and might be the involvement of caspase-3 activation and ROS production.
汤光耀, 姜玉峰, 吕海龙, 李佳洁, 杨仁坦, 秦文娟, 马斌, 马容基, 王麟尧, 陈琳, 许雅. 甘氨鹅脱氧胆酸对体外细粒棘球蚴原头节活力及ROS影响[J]. 中国人兽共患病学报, 2018, 34(7): 595-598.
TANG Guang-yao, JIANG Yu-feng, LYU Hai-long, LI Jia-jie, YANG Ren-tan, QIN Wen-juan, MA Bin, MA Rong-ji, WANG Lin-yao, CHEN Lin, XU Ya. In vitro effect of glycoglycochenodeoxycholic acid on viability and reactive oxygen species in Echinococcus granulosus protoscoleces. Chinese Journal of Zoonoses, 2018, 34(7): 595-598.
[1] Moro P, Schantz PM.Cystic echinococcosis in the Americas[J]. Parasitol Int, 2006, 55(Suppl 1):S181-186. [2] Ammann R W, Eckert J.Cestodes. Echinococcus[J]. Gastroenterol Clin North America, 1996, 25(3):655-659. [3] Safioleas MC, Misiakos EP, Kouvaraki M, et al.Hydatid disease of the liver: a continuing surgical problem[J]. Arch surgery, 2006, 141(11):1101-1108. [4] Sharma R, Majer F, Peta VK, et al.Bile acid toxicity structure-activity relationships: correlations between cell viability and lipophilicity in a panel of new and known bile acids using an oesophageal cell line (HET-1A)[J]. Bioorgan Med Chemistry, 2010,18(18): 6886-6895. [5] Goldberg AA, Titorenko VI, Beach A, et al.Bile acids induce apoptosis selectively in androgen-dependent and -independent prostate cancer cells[J]. Peerj, 2013, 1(21):e122-138. [6] Kern P. Medical treatment of echinococcosis under the guidance of Good Clinical Practice(GCP/ICH).[J]. ParasitolInternat, 2006, 55 Suppl(Suppl.):S273-282. [7] Horton RJ.Albendazole in treatment of human cystic echinococcosis: 12 years of experience.[J]. Acta Tropica, 1997, 64(1/2):79-93. [8] López d SI, Olmo N, Turnay J, et al. Acquisition of resistance to butyrate enhances survival after stress and induces malignancy of human colon carcinoma cells.[J]. Cancer Res, 2004, 64(13):4593-4600. [9] Gafar AA, Draz HM, Goldberg AA, et al.Lithocholic acid induces endoplasmic reticulum stress, autophagy and mitochondrial dysfunction in human prostate cancer cells[J]. Peerj, 2016, 4(1):e2445-2466. [10] Bernstein H, Bernstein C, Payne CM, et al.Bile acids as carcinogens in human gastrointestinal cancers[J]. Mutation Res, 2005, 589(1):47-65. [11] Thomas C, Pellicciari R, Pruzanski M, et al.Targeting bile-acid signalling for metabolic diseases.[J]. Nat Rev Drug Discovery, 2008, 7(8):678-693. [12] Dai J, Wang H, Dong Y, et al.Bile acids affect the growth of human cholangiocarcinoma via NF-kB pathway[J]. Cancer Invest, 2013, 31(2):111-120. [13] Shi H, Lei Y, Wang B, et al.Protoscolicidal effects of chenodeoxycholic acid on protoscoleces of Echinococcus granulosus[J]. Exper Parasitol, 2016, 167:76-82. [14] Victor VM, Mccreath KJ, Rocha M.Recent progress in pharmacological research of antioxidants in pathological conditions: cardiovascular health[J]. Recent Pat Antiinf Drug Discov, 2006, 1(1):17-31. [15] Schumacker PT.Reactive oxygen species in cancer cells: Live by the sword, die by the sword[J]. Cancer Cell, 2006, 10(3):175-176. [16] Guo CL, Wang LJ, Zhao Y, et al.A novel bromophenol derivative BOS-102 induces cell cycle arrest and apoptosis in human A549 lung cancer cells via ROS-Mediated PI3K/Akt and the MAPK Signaling Pathway[J]. Marine Drugs, 2018, 16(2):43. [17] Lei L, Huang L, Huang T, et al.Cell-penetrating peptide conjugates of gambogic acid enhance the antitumor effect on human bladder cancer EJ cells through ROS-mediated apoptosis[J]. Drug Design Develop Therapy, 2018, 12:743-756.