1.Department of Pharmacy, Shenzhen Center for Chronic Disease Prevention and Control, Guangdong Province, Shenzhen 518020, China;
2.Institute of Respiratory Diseases, Guangdong Medical University, Guangdong Province, Zhanjiang 524023, China;
3.Department of Biochemistry and Molecular Biology, Guangdong Medical University, Zhanjiang , Guangdong 524023, China
Abstract：Objective To investigate the effects of Naringenin on the proliferation, apoptosis and cell cycle of human lung squamous cell carcinoma cell line NCI-H2170. Methods The proliferation of NCI-H2170 cells was detected by MTT assay. The morphological changes of NCI-H2170 cells were detected by Hoechst33258/PI staining. Cell cycle changes were measured by flow cytometry (FCM). Western blot was used to detect the expression of PARP, Bid, Bcl-2, procaspase-3 and procaspase-8 in NCI-H2170 cells treated with naringenin. Results The proliferation of human lung squamous cell carcinoma NCI-H2170 cells were inhibited in a dose-dependent manner after treating with Naringenin for 24 h. It was not significant difference between 12.5 μmol/L treatment group and the control group (P > 0.05).However, 25, 50, 100 μmol/L treatment groups were significantly different comparing to the control group (P < 0.05). The results of flow cytometry analysis showed that it was not significant difference between 12.5 μmol/L treatment group and the control group (P > 0.05). However, after NCI-H2170 cells were treated with 25, 50, 100 μmol/L naringenins, the number of cells had significantly increased in G1 phase, desceased in S phase and G2 phase, comparing to the control group (P < 0.05). Naringenin up-regulated Bid expression, promoted the degradation of PARP and the decrease of Bcl-2, proaspase-3 and proaspase-8 in NCI-H2170 cells, comparing to the control group (P < 0.05). Conclusion Naringenin inhibits the proliferation of human lung squamous cell carcinoma cell line NCI-H2170 and induces the G1 phase arrest in NCI-H2170 cells and induces cell apoptosis.
[1] Noder G，Arco C，Fusco D，et al. Preoperative assessment and risk factors in the surgical treatment of lung cancer：the role of age [J]. Rays，2004，29（4）：407-411.
[2] 汤兆猷.现代肿瘤学[J].2版.上海：上海医科大学出版社，2000.
[3] Fang T，Wang T，Ma Y，et al. A rapid LC/MS/MS quantitation assay for naringin and its two metabolites in rats plasma [J]. J Pharm Biomed Anal，2006，40（2）：454-459.
[4] Tripoli E，La Guardia M，Giammanco S，et al. Citrus flavonoids：molecular structure，biological activity and nutritional properties：a review [J]. Food Chem，2007，104（2）：466-479
[5] Park HJ，Choi YJ，Lee JH，et al. Naringenin causes ASK1-induced apoptosis via reactive oxygen species in human pancreatic cancer cells [J]. Food Chem Toxicol，2017，99：1-8.
[6] Lim W，Park S，Bazer FW，et al. Naringenin-induced apoptotic cell death in prostate cancer cells is mediated via the PI3K/AKT and MAPK signaling pathways [J]. J Cell Biochem，2017，118（5）：1118-1131.
[7] Zhang F，Dong W，Zeng W，et al. Naringenin prevents TGF-β1 secretion from breast cancer and suppresses pulmonary metastasis by inhibiting PKC activation [J]. Breast Cancer Res，2016，18（1）：38.
[8] Wang X，Ge J，Wang K，et al. Evaluation of MTT assay for measurement of emodin-Induced cytotoxicity [J]. Assay Drug Dev Technol，2006，4（2）：203-207.
[9] 孙艳红，沈玉梅.中药对肿瘤放射性治疗增敏作用的研究进展[J].上海中医药杂志，2007，41（6）：82-84.
[10] Banjerdpongchai R，Wudtiwai B，Khawon P. Induction of human hepatocellular carcinoma HepG2 cell apoptosis by naringin [J]. Asian Pac J Cancer Prev，2016，17（7）：3289-3294.
[11] Wei K，Xie Y，Chen T，et al. ERK1/2 signaling mediated naringin-induced osteogenic differentiation of immortalized human periodontal ligament stem cells [J]. Biochem Biophys Res Commun，2017，489（3）：319-325.
[12] Cai Z，Liu Q. Cell cycle regulation in treatment of breast cancer [J]. Adv Exp Med Biol，2017，1026：251-270.
[13] Mills CC，Kolb EA，Sampson VB. Development of chemotherapy with cell-cycle inhibitors for adult and pediatric cancer therapy [J]. Cancer Res，2018，78（2）：320-325.
[14] Lee H，Shin EA，Lee JH，et al. Caspase inhibitors：a review of recently patented compounds（2013-2015）[J]. Expert Opin Ther Pat，2018，28（1）：47-59.
[15] Cho YS，Park HL. Exploitation of necroptosis for treatment of caspase-compromised cancers [J]. Oncol Lett，2017， 14（2）：1207-1214.
[16] Kale J，Osterlund EJ，Andrews DW. BCL-2 family proteins：changing partners in the dance towards death [J]. Cell Death Differ，2018，25（1）：65-80.
[17] Deng J. How to unleash mitochondrial apoptotic blockades to kill cancers？[J] Acta Pharm Sin B，2017，7（1）：18-26.
[18] Kaufmann T，Strasser A，Jost PJ. Fas death receptor signalling：roles of Bid and XIAP [J]. Cell Death Differ，2012， 19（1）：42-50.
[19] Brown JS，O'Carrigan B，Jackson SP，et al. Targeting DNA repair in cancer：beyond PARP inhibitors [J]. Cancer Discov，2017，7（1）：20-37.
[20] Lyakhovich A，Surralles J. Constitutive activation of caspase-3 and poly ADP ribose polymerase cleavage in Fanconi Anemia Cells [J]. Mol cancer Res，2010，8（1）：46-56.
2018, Vol. 15 
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