بررسی اثر کورکومین بر محافظت عصبی در مدل سلولی بیماری پارکینسون القاء شده با سم 6– هیدروکسی دوپامین
محورهای موضوعی : فصلنامه زیست شناسی جانوریمهدیه آذرشب 1 , رامین حاجی خانی 2 , مهدی رهنما 3 , محمدرضا بیگدلی 4 , جلال صولتی 5
1 - گروه زیست شناسی، واحد تهران شمال، دانشگاه آزاد اسلامی، تهران، ایران
2 - گروه زیست شناسی، واحد تهران شمال، دانشگاه آزاد اسلامی، تهران، ایران
3 - گروه زیست شناسی، واحد زنجان، دانشگاه آزاد اسلامی، زنجان، ایران
4 - گروه زیست شناسی، دانشکده علوم زیستی، دانشگاه شهید بهشتی، تهران، ایران
5 - گروه زیست شناسی، واحد کرج، دانشگاه آزاد اسلامی، کرج، ایران
کلید واژه: کورکومین, پارکینسون, سلول کاتکول آمینرژیک, 6– هیدروکسی دوپامین,
چکیده مقاله :
بیماری پارکینسون یکی از شایع ترین انواع بیماری های نورودژنراتیو است که با اختلالات حرکتی مانند کندی حرکت، فقدان حرکت، سختی عضلانی و لرزش در حال استراحت و کاهش قدرت صدا مشخص می شود. علت اصلی بیماری، تخریب نورون های دوپامینرژیک بخش متراکم جسم سیاه در مغز میانی و کاهش غلظت دوپامین در پایانه های جسم مخطط است. این مطالعه، به منظور بررسی اثر کورکومین بر مدل سلولی بیماری پارکینسون القاء شده با سم 6-هیدروکسی دوپامین با هدف کاهش التهاب سلولی انجام شد. محیط کشت مورد استفاده در این مطالعهFBS+DMEM 10 درصد برای مطالعه سلول های کاتکول آمینرژیک می باشد. برای ایجاد مدل سلولی پارکینسون از سم 6- هیدروکسی دوپامین استفاده شد. از دوزهای20، 25 و 30 میلی گرم بر کیلوگرم کورکومین به عنوان دارو و برای شمارش سلول های زنده از دو روش رنگ آمیزیMTT و BT استفاده شد. نتایج مطالعه حاضر، نشان دادکه مصرف کورکومین می تواند منجربه افزایش توان آنتی اکسیدانتی وحافظت سلول از آسیب های ناشی از بنیان های فعال اکسیژن گردد. درمان باکورکومین به جهت خاصیت ضدالتهابی، با توجه به نتایج آزمون MTT و BT نیز نشان داد که حفاظت سلولی افزایش، مرگ سلول های کاتکول آمینرژیک توسط سم 6 – هیدروکسی دوپامین به صورت معناداری کاهش یافته است. که نشان دهنده اثرات آنتی اکسیدانتی و ضدالتهابی کورکومین، در برابر آسیب های ناشی از بیماری پارکینسون و کاهش پیشرفت علایم بیماری می باشد.
Parkinson's disease is one of the most common types of the neurodegenerative disease, which is characterized by the movement disorders such as slowness, lack of movement, muscle stiffness, and resting tremor, and hypophonic. The main reason of disease is the destruction of dopaminergic neurons in the Substantia Nigra in the midbrain and a decrease in dopamine concentration in the striatum terminals. In this study, used culture medium was DMEM with FBS, and the cells under study were catecholaminergic cells.6-Hydroxy dopamine toxin was used on cells to create a Parkinson cell model. Curcumin was used as a drug, and MTT, and BT methods were used to count the living cells. This research was designed to study the curcumin effect on Parkinson's disease with cellular model induced by 6-Hydroxy dopamine toxin with reduced inflammation. This study's results showed that using curcumin can increase the antioxidant power and protect the cell from damage caused by reactive oxygen species. Due to the results of MTT, and curcumin treatment due to its anti-inflammatory properties BT test also showed that cellular protection had increased, the death of aminergic catechol cells by 6-hydroxy dopamine toxin was significantly reduced. It shows the antioxidant and anti-inflammatory effects of curcumin on the damage caused by Parkinson's disease and reducing the progression of symptoms. Treatment withcurcumin to be anti-inflammatory can reduce the death of catecholaminergic cells by 6-hydroxy dopamine toxin.
1- Aggarwal B.B., Sundaram C., Malani N., Ichikawa H. 2007. Curcumin: In The molecular targets and therapeutic uses of curcumin in health and disease. The Indian Solid Gold, 5(1): 69-75.
2- Ammon H., Safayhi H., Mack T., Sabieraj J. 1993. Mechanism of antiinflammatory actions of curcumine and boswellic acids. Journal of Ethnopharmacology, 38(2): 105-112.
3- Araujo C., Leon L. 2001. Biological activities of Curcuma longa L. Memórias do Instituto Oswaldo Cruz, 9(3): 723-728.
4- Aslantürk ÖS., 2017. In Vitro Cytotoxicity and Cell Viability Assays Principles, Advantages, and Disadvantages. InTech. 71923
5- Berry C., La Vecchia C., Nicotera P., 2010. Paraquat and Parkinson's disease. Cell Death and Differentiation, 17(3): 1115.
6- Blum D., Torch S., Lambeng N., Nissou M.F., Benabid A.L., Sadoul R., Verna J.M. 2001. Molecular pathways involved in the neurotoxicity of 6-OHDA dopamine and MPTP contribution to the apoptotic theory in Parkinson's disease. Progress in Neurobiology, 65(4): 135-172.
7- Cho J.W., Lee K.S., Kim C.W. 2007. Curcumin attenuates the expression of IL-1β, IL-6, and TNF-α as well as cyclin E in TNF-α-treated HaCaT cells; NF-κB and MAPKs as potential upstream targets. International Journal of Molecular Medicine, 19(2): 469-474.
8- Collins L.M., Toulouse A., Connor T.J., Nolan Y.M. 2012. Contributions of central and systemic inflammation to the pathophysiology of Parkinson’s disease. Neuropharmacology, 62(4): 2154-2168.
9- Elbaz A., Bower J.H., Maraganore D.M., McDonnell S.K., Peterson B.J., Ahlskog J.E., Schaid D.J., Rocca W.A. 2002. Risk tables for parkinsonism and Parkinson's disease. Journal of Clinical Epidemiology, 5(3): 25-31.
10- Ferrari C.C., Tarelli R. 2011. Parkinson’s disease and systemic inflammation. Foundation PD. Parkinson’s Statistics,10(4): 4061-4072
11- Francis D., Rapid R.L. 1986. Colorometric assay for cell growth and survival: modifications to the tetrazolium dye procedure giving improved sensitivity and reliability. Journal of Immunological Methods, 89(3): 271-277.
12- Gupta S. C., Kim J. H., Prasad S., Aggarwal B.B. 2010. Regulation of survival, proliferation, invasion, angiogenesis, and metastasis of tumor cells through modulation of inflammatory pathways by nutraceuticals. Cancer Metastasis Review, 29(3): 405–434.
13- Hasanzadeh SH., Bonyady F. 2017. Principles and methods of animal cell culture. Urmia University, 237-289.]in persian[
14- Hayon T., Dvilansky A., Shpilberg O., Nathan I. 2003.Appraisal of the MTT-based assay as a useful tool for predicting drug chemosensitivity in leukemia. Leukemia and Lymphoma, 44(11): 1957-1962.
15- Hong J., Bose M., Ju J., Ryu J.H., Chen X., Sang S., Lee M. J., Yang C.S. 2004. Modulation of arachidonic acid metabolism by curcumin and related β-diketone derivatives: effects on cytosolic phospholipase A 2, cyclooxygenases and 5-lipoxygenase. Carcinogenesis, 25(2): 1671-1679.
16- Huang M. T., Lysz T., Ferraro T., Abidi T.F., Laskin J.D., Conney A.H. 1991. Inhibitory effects of curcumin on in vitro lipoxygenase and cyclooxygenase activities in mouse epidermis. Cancer Research, 5(1): 813-819.
17- Hubble JP., Cao T., Hassanein R., Neuberger J., Roller W., 1993. Risk factors for Parkinson's disease. Neurology, 43(3): 1693-1693.
18- Jobin C., Bradham C.A., Russo M.P., Juma B., Narula A.S., BrennerD.A., Sartor R.B., 1999. Curcumin blocks cytokine-mediated NF-κB activation and proinflammatory gene expression by inhibiting inhibitory factor I-κB kinase activity. The Journal of Immunology, 163(6): 3474-3483.
19- Lin T.K., Liou C.W., Chen S.D., Chuang Y.C., Tiao M.M., Wang P.W., Chen J.B., Chuang J.H., 2009. Mitochondrial dysfunction and biogenesis in the pathogenesis of Parkinson’s disease. Chang Gung Medical Journal, 32(3): 589-599.
20- Maheshwari R.K., Singh A.K., Gaddipati J., Srimal R.C., 2006. Multiple biological activities of curcumin: a short review. Life Sciences, 78(4): 2081-2087.
21- McGeer P.L., McGeer E.G., 2004. Inflammation and neurodegeneration in Parkinson's disease. Parkinsonism & related disorders, 10(3): S32-S37.
22- Moken Y., Xianping D., Yaoshu T. 1984. Studies on the chemical constituents of common turmeric (Curcuma longa). Zhongcoayoa, 15(3): 197-198.
23- Moldeus T., Hogberg J., Orrhenius S., Fleischer S., Packer L.,1978. Trypan blue dye exclusion method. Meth Enzym, 5(2): 60-71.
24- Motterlini R., Clark J.E., Foresti R., Sarathchandra P., Mann B.E., Green C.J. 2002. Carbon monoxide-releasing molecules characterization of biochemical and vascular activities. Circulation Research, 90(2): 17-24.
25- Ono K., Hasegawa K., Naiki H., Yamada M. 2004. Curcumin has potent anti‐amyloidogenic effects for Alzheimer's β‐amyloid fibrils in vitro. Journal of Neuroscience Research, 75(4): 742-750.
26- Philip S., Kundu G.C. 2003. Osteopontin induces nuclear factor-kB-mediated promatrix metalloproteinase-2 activation through IkB alpha/IKK signaling pathways and curcumin (Diferulolylmethane) down regulates these pathways. Journal of Biological Chemistry, 278(16): 1487-1497.
27- Pulido-Moran M., Moreno-Fernandez J., Ramirez-Tortosa C., Ramirez-Tortosa M. 2016. Curcumin and health. Molecules, 21(3): 264-273.
28- Sahu A., Kasoju N., and Bora U., 2008. Fluorescence study of the curcumin− casein micelle complexation and its application as a drug nanocarrier to cancer cells. Biomacromolecules ,9(3): 2905-2912.
29- Samiei A., Tabatabaei-Yazdi F., Mazaheri Tehrani M., 2017. An investigation into the antioxidant activity, phenolic compounds, antimicrobial effect and interaction of the essential oils of Curcuma longa and Ocimum basilicum on some pathogenic bacteria. Food Science and Technology, Faculty of Agriculture, Ferdowsi University of Mashhad, 74(15): 99 -107.]in persian [
30- Savica R., Rocca W.A., Ahlskog J.E. 2010. When does Parkinson disease start? Archives of neurology, 67(3): 798-801.
31- Schapira A.H. 2009. Neurobiology and treatment of Parkinson's disease. Trends in pharmacological sciences, 30(3): 41-47.
32- Sikora E., Scapagnini G., and Barbagallo M., 2010. Curcumin, inflammation, ageing and age-related diseases. Immunity & Ageing, 7(1): 12-18.
33- Thoenen H., Tranzer J. 1968. Chemical sympathectomy by selective destruction of adrenergic nerve endings with 6-hydroxydopamine. Naunyn-Schmiedebergs Archiv für Pharmakologie und Experimentelle Pathologie, 261(3): 271-288.
34- Tomita M., Kawakami H., Uchihara J. n., Okudaira T., Masuda M., Takasu N., Matsuda T., Ohta T., Tanaka Y., Ohshiro K. 2006. Curcumin (diferuloylmethane) inhibits constitutive active NF-kappaB, leading to suppression of cell growth of human T-cell leukemia virus type I-infected T-cell lines and primary adult T-cell leukemia cells. International Journal of Cancer, 118(4): 765-772.
35- Veldman B., Wijn A., Knoers N., Praamstra P., Horstink M. 1998. Genetic and environmental risk factors in Parkinson’s disease. Clinical Neurology and Neurosurgery, 100(4): 15-26.
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