{"title":"Apoptosis Activity of Persea declinata (Bl.) Kosterm Bark Methanolic Crude Extract","authors":"P. Narrima, C. Y. Looi, M. A. Mohd, H. M. Ali","volume":93,"journal":"International Journal of Pharmacological and Pharmaceutical Sciences","pagesStart":664,"pagesEnd":670,"ISSN":"1307-6892","URL":"https:\/\/publications.waset.org\/pdf\/9999704","abstract":"
Persea declinata (Bl.) Kosterm is a member of the
\r\nLauraceae family, widely distributed in Southeast Asia. It is from the
\r\nsame genus with avocado (Persea americana Mill), which is widely
\r\nconsumed as food and for medicinal purposes. In the present study,
\r\nwe examined the anticancer properties of Persea declinata (Bl.)
\r\nKosterm bark methanolic crude extract (PDM). PDM exhibited a
\r\npotent antiproliferative effect in MCF-7 human breast cancer cells,
\r\nwith an IC50 value of 16.68 .g\/mL after 48h of treatment. We
\r\nobserved that PDM caused cell cycle arrest and subsequent apoptosis
\r\nin MCF-7 cells, as exhibited by increased population at G0\/G1 phase,
\r\nhigher lactate dehydrogenase (LDH) release, and DNA
\r\nfragmentation. Mechanistic studies showed that PDM caused
\r\nsignificant elevation in ROS production, leading to perturbation of
\r\nmitochondrial membrane potential, cell permeability, and activation
\r\nof caspases-3\/7. On the other hand, real-time PCR and Western blot
\r\nanalysis showed that PDM treatment increased the expression of the
\r\nproapoptotic molecule, Bax, but decreased the expression of
\r\nprosurvival proteins, Bcl-2 and Bcl-xL, in a dose-dependent manner.
\r\nThese findings imply that PDM could inhibit proliferation in MCF-7
\r\ncells via cell cycle arrest and apoptosis induction, indicating its
\r\npotential as a therapeutic agent worthy of further development.<\/p>\r\n","references":"[1] K. H. Lee, \u201cAntineoplastic agents and their analogues from Chinese\r\ntraditional medicine,\u201d in HumanMedicinal Agents from Plants, A. D.\r\nKinghorn andM. Balandrin, Eds., vol. 534 of ACS Symposium Series,\r\npp. 170\u2013190, American Chemical Society, Washington, DC, USA, 1993.\r\n[2] K.-H. Lee, \u201cAnticancer drug design based on plant-derived natural\r\nproducts,\u201d Journal of Biomedical Science, vol. 6, no. 4, pp. 236\u2013250,\r\n1999.\r\n[3] H. Ding, Y.-W. Chin, A. D. Kinghorn, and S. M. D\u2019Ambrosio,\r\n\u201cChemopreventive characteristics of avocado fruit,\u201d Seminars in Cancer\r\nBiology, vol. 17, no. 5, pp. 386\u2013394, 2007.\r\n[4] V. R.Gummadi, S. Rajagopalan, C.Y. Looi et al., \u201cDiscovery of 7-\r\nazaindole based anaplastic lymphoma kinase (ALK) inhibitors: wild\r\ntype and mutant (L1196M) active compounds with unique binding\r\nmode,\u201d Bioorganic & Medicinal Chemistry Letters, vol. 23, no. 17, pp.\r\n4911\u20134918, 2013.\r\n[5] C. Y. Looi, M. Imanishi, S. Takaki et al., \u201cOcta-Arginine mediated\r\ndelivery of wild-type Lnk protein inhibits TPO-induced M-MOK\r\nmegakaryoblastic leukemic cell growth by promoting apoptosis,\u201d PLoS\r\nONE, vol. 6, no. 8, article e23640, 2011.\r\n[6] C. Y. Looi, B. Moharram, M. Paydar et al., \u201cInduction of apoptosis in\r\nmelanoma A375 cells by a chloroform fraction of Centratherum\r\nanthelminticum (L.) seeds involves NF-kappaB, p53 and Bcl-2-\r\ncontrolled mitochondrial signaling pathways,\u201d BMC Complementary\r\nand Alternative Medicine, vol. 13, article 166, 2013.\r\n[7] R. S. Ahmed, S. G. Suke, V. Seth, A. Chakraborti, A. K. Tripathi, and\r\nB.D. Banerjee, \u201cProtective effects of dietaryginger (Zingiber officinales\r\nRose) on lindane-induced oxidative stress in rats,\u201d Phytotherapy\r\nResearch, vol. 22, no. 7, pp. 902\u2013906, 2008.\r\n[8] R. S. Ahmed, S. G. Suke, V. Seth, A. Chakraborti, A. K. Tripathi, and\r\nB.D. Banerjee, \u201cProtective effects of dietaryginger (Zingiber officinales\r\nRose) on lindane-induced oxidative stress in rats,\u201d Phytotherapy\r\nResearch, vol. 22, no. 7, pp. 902\u2013906, 2008.\r\n[9] A. S. Naura and R. Sharma, \u201cToxic effects of hexaammine cobalt (III)\r\nchloride on liver and kidney in mice: implication of oxidative stress,\u201d\r\nDrug and Chemical Toxicology, vol. 32, no. 3, pp. 293\u2013299, 2009.\r\n[10] J M. Germain, E. B. Affar, D. D\u2019Amours, V. M. Dixit, G. S. Salvesen,\r\nand G. G. Poirier, \u201cCleavage of automodified poly(ADP-ribose)\r\npolymerase during apoptosis. Evidence for involvement of caspase-7,\u201d\r\nThe Journal of Biological Chemistry, vol. 274, no. 40, pp. 28379\u201328384,\r\n1999.\r\n[11] S. Shimizu, Y. Eguchi, W. Kamiike et al., \u201cBcl-2 blocks loss of\r\nmitochondrial membrane potential while ICE inhibitors act at a different\r\nstep during inhibition of death induced by respiratory chain inhibitors,\u201d\r\nOncogene, vol. 13, no. 1, pp. 21\u201329, 1996.\r\n[12] J. Yang, X. Liu, K. Bhalla et al., \u201cPrevention of apoptosis by Bcl2:\r\nrelease of cytochrome c frommitochondria blocked,\u201d Science, vol. 275,\r\nno. 5303, pp. 1129\u20131132, 1997.\r\n[13] Y. Hu, M. A. Benedict, D. Wu, N. Inohara, and G. Nunez, \u201cBcl-XL\r\ninteracts with Apaf-1 and inhibits Apaf-1-dependent caspase-9\r\nactivation,\u201d Proceedings of the National Academy of Sciences of the\r\nUnited States of America, vol. 95, no. 8, pp. 4386\u20134391, 1998.","publisher":"World Academy of Science, Engineering and Technology","index":"Open Science Index 93, 2014"}