بررسی اثر بتاآسارون بر غلظت فاکتور نکروز توموری- آلفا در مدل موش صحرایی آلزایمری‌شده
الموضوعات :
گلشید ساکی
1
(دانش‌آموخته دکترای تخصصی گروه زیست شناسی، دانشکده علوم پایه، واحد علوم و تحقیقات فارس، دانشگاه آزاد اسلامی، فارس، ایران؛ دانش‌آموخته دکترای تخصصی گروه زیست شناسی، دانشکده علوم، کشاورزی و فن‌آوری‌های نوین، واحد شیراز، دانشگاه آزاد اسلامی، شیراز، ایران.)
اکرم عیدی
2
(استاد گروه زیست شناسی، دانشکده علوم پایه، واحد علوم و تحقیقات، دانشگاه آزاد اسلامی، تهران، ایران.)
سید پژمان مرتضوی
3
(دانشیار گروه پاتولوژی، دانشکده علوم تخصصی دامپزشکی، واحد علوم و تحقیقات، دانشگاه آزاد اسلامی، تهران، ایران.)
اکبر وحدتی
4
(استاد گروه زیست شناسی، دانشکده علوم پایه، واحد علوم و تحقیقات فارس، دانشگاه آزاد اسلامی، فارس، ایران؛ استاد گروه زیست شناسی، دانشکده علوم، کشاورزی و فن‌آوری‌های نوین، واحد شیراز، دانشگاه آزاد اسلامی، شیراز، ایران.)
نگار پناهی
5
(استادیار گروه علوم پایه، دانشکده علوم تخصصی دامپزشکی، واحد علوم و تحقیقات، دانشگاه آزاد اسلامی، تهران، ایران.)
تاريخ الإرسال : 29 الثلاثاء , ربيع الثاني, 1439
تاريخ التأكيد : 15 الأربعاء , صفر, 1440
تاريخ الإصدار : 09 الأربعاء , رمضان, 1442
الکلمات المفتاحية:
موش صحرایی,
آلزایمر,
بتاآسارون,
بتا‌آمیلویید,
فاکتور نکروز توموری- آلفا,
ملخص المقالة :
بتا آسارون ماده موثره گیاه Acorus tatarinowii Schott می باشد که قادر به عبور از سد خونی مغز بوده و بر سیستم اعصاب مرکزی تاثیر می گذارد. در تحقیق حاضر اثر بتا آسارون بر غلظت فاکتور نکروز توموری- آلفا (TNF-α) به دنبال دریافت بتا آمیلویید در مغز موش های صحرایی نر بالغ مورد بررسی قرار گرفت. موش های صحرایی نر بالغ به صورت تصادفی به 9 گروه 6 تایی تقسیم شدند: گروه کنترل سالم، گروه شاهد جراحی، گروه های دریافت کننده بتا آسارون (5/12، 25 و 50 میلی گرم بر کیلوگرم وزن بدن به صورت خوراکی به مدت 50 روز)، گروه کنترل آلزایمری (دریافت کننده یک دوز 4 میکرولیتری بتا آمیلویید 42-1 به صورت تزریق دو طرفه در هیپوکامپ) و گروه های آلزایمری شده و دریافت کننده بتا آسارون (تیمار دوزهای 5/12، 25 و 50 میلی گرم بر کیلوگرم وزن بدن بتا آسارون به صورت خوراکی به مدت 30 روز و بعد از دریافت بتا آمیلویید، ادامه تیمار با بتا آسارون به مدت 3 هفته). در پایان آزمایش حیوانات کشته شدند و غلظت TNF-α در هموژنات مغز اندازه گیری گردید. تیمار بتا آسارون در دوزهای 25 و 50 میلی گرم بر کیلوگرم وزن بدن، موجب کاهش غلظت TNF-α در موش های صحرایی آلزایمری شده گردید(001/0p <). با توجه به یافته های حاصل از این مطالعه می توان نتیجه گیری کرد که بتا آسارون در محافظت در برابر التهاب حاصل از دریافت بتا آمیلویید در بافت مغز موش صحرایی نقش موثری ایفا می کند.
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Alderton, W.K., Cooper, C.E. and Knowles, R.G. (2001). Nitric oxide synthases: structure, function and inhibition. Biochemical Journal, 357(3): 593-615.
Alvarez, A., Cacabelos, R., Sanpedro, C., Garcia-Fantini, M. and Aleix-andre, M. (2007). Serum TNF-alpha levels are increased and correlate negatively with free IGF-I in Alzheimer disease. Neurobiology of Aging, 28(4): 533-536.
Ansari, N. and Khodagholi, F. (2013). Natural products as promising drug candidates for the treatment of Alzheimer’s disease: molecular mechanism aspect. Current Neuropharmacology, 11(4): 414-429.
Bertram, L., Lill, C.M. and Tanzi, R.E. (2010). The genetics of Alzheimer disease: back to the future. Neuron, 68(2): 270-281.
Chang, W. and Teng, J. (2015). β-asarone prevents Aβ25-35-induced inflammatory responses and autophagy in SH-SY5Y cells: down expression Beclin-1, LC3B and up expression Bcl-2. International Journal of Clinical and Experimental Medicine, 8(11): 20658-20663.
Chen, X., Walker, D.G., Schmidt, A.M., Arancio, O., Lue, L.F. and Yan, S.D. (2007). RAGE: a potential target for Abeta-mediated cellular perturbation in Alzheimer’s disease. Current Molecular Medicine, 7(8): 735-742.
Chen, Y.Z., Wang, Q.W., Liang, Y. and Fang, Y.Q. (2007). Protective effects of beta-asarone on cultured rat cortical neurons damage induced by glutamate. Zhong Yao Cai, 30(4): 436-438.
Cho, J., Kim, Y.H., Kong, J.Y., Yang, C.H. and Park, C.G. (2002). Protection of cultured rat cortical neurons from excitotoxicity by asarone, a major essential oil component in the rhizomes of Acorus gramineus. Life Sciences, 71(5): 591-599.
Chun, H.S., Kim, J.M., Choi, E.H. and Chang, N. (2008). Neuroprotective effects of several Korean medicinal plants traditionally used for stroke remedy. Journal of Medical Food, 11(2): 246-251.
Dobarro, M., Orejana, L., Aguirre, N. and Ramírez, M.J. (2013). Propranolol reduces cognitive deficits, amyloid β levels, tau phosphorylation and insulin resistance in response to chronic corticosterone administration. International Journal of Neuropsychopharmacology, 16(6): 1351-1360.
Fan, R., Xu, F., Previti, M.L., Davis, J., Grande, A.M., Robinson, J.K., et al. (2007). Minocycline reduces microglial activation and improves behavioral deficits in a transgenic model of cerebral microvascular amyloid. Journal of Neuroscience, 27(12): 3057-3063.
Fang, F., Lue, L.F., Yan, S., Xu, H., Luddy, J.S., Chen, D., et al. (2010). RAGE-dependent signaling in microglia contributes to neuroinflammation, Abeta accumulation, and impaired learning/memory in a mouse model of Alzheimer’s disease. The FASEB Journal, 24(4): 1043-1055.
Fang, Y.Q., Fang, R.M., Fang, G.L., Jiang, Y. and Fu, S.Y. (2008). Effects of beta-asarone on expression of c-fos in kindling epilepsy rat brain. Zhongguo Zhong Yao Za Zhi, 33(5): 534-536.
Fang, Y.Q., Li, L. and Wu, Q.D. (2003). Effects of beta-asarone on gene expression in mouse brain. Zhong Yao Cai, 26(9): 650-652.
Fang, Y.Q. and Wei, G. (2002). To analyze if the Rhizoma Acori Tatarimowii naph-tha can go through the BBB or not with GC-MS. Zhong Yao Xin Yao Yu: Ling Chuang Yao Li, 13(3): 181-182.
Fu, S.Y., Fang, R.M., Fang, G.L., Xie, Y.H. and Fang, Y.Q. (2008). Effects of beta-asarone on expression of FOS and GAD65 in cortex of epileptic rat induced by penicillin. Zhong Yao Cai, 31(1): 79-81.
Geng, Y., Li, C., Liu, J., Xing, G., Zhou, L., Dong, M., et al. (2010). Beta-asarone improves cognitive function by suppressing neuronal apoptosis in the beta-amyloid hippocampus injection rats. Biological and Pharmaceutical Bulletin, 33(5): 836-843.
Han, L., Yin, K., Zhang, S., Wu, Z., Wang, C., Zhang, Q., et al. (2013). Dalesconols B inhibits lipopolysaccharide induced inflammation and suppresses NF-kappaB and p38/JNK activation in microglial cells. Neurochemistry International, 62(7): 913-921.
Huang, L., Deng, M., He, Y. and Fang, Y. (2015). β-asarone and levodopa coadministration protects against 6-OHDA-induced damage in parkinsonian rat mesencephalon by regulting autophagy: down expression Beclin-1 and LC3B and up expression p62. Clinical and Experimental Pharmacology and Physiology, 42(3): 269-277.
Imbimbo, B.P., Lombard, J. and Pomara, N. (2005). Pathophysiology of Alzheimer's disease. Neuroimaging Clinics of North America, 15(4): 727-753.
Jayasooriya, R.G., Kang, C.H., Seo, M.J., Choi, Y.H., Jeong, Y.K. and Kim, G.Y. (2011). Exopolysaccharide of Laetiporus sulphureus var. miniatus down regulates LPS-induced production of NO, PGE(2), and TNF-alpha in BV2 microglia cells via suppression of the NF-kappaB pathway. Food and Chemical Toxicology, 49(11): 2758-2764.
Jean, Y.Y., Baleriola, J., Fà, M., Hengst, U. and Troy, C.M. (2015). Stereotaxic infusion of oligomeric Amyloid-beta into the mouse hippocampus. Journal of Visualized Experiments, 100(6): e52805.
Kang, C.H., Jayasooriya, R.G., Dilshara, M.G., Choi, Y.H., Jeong, Y.K., Kim, N.D., et al. (2012). Caffeine suppresses lipopolysaccharide-stimulated BV2 microglial cells by suppressing Akt-mediated NF-kappaB activation and ERK phosphorylation. Food and Chemical Toxicology, 50(12): 4270-4276.
Klein, R.L., Dayton, R.D., Diaczynsky, C.G. and Wang, D.B. (2010). Pronounced micro gliosis and neurodegeneration in aged rats after tau gene transfer. Neurobiology of Aging, 31(12): 2091-2102.
Lee, B., Sur, B., Cho, S.G., Yeom, M., Shim, I., Lee, H., et al. (2015). Effect of Beta-Asarone on impairment of spatial working memory and apoptosis in the hippocampus of rats exposed to chronic corticosterone administration. Biomolecules and Therapeutics (Seoul), 23(6): 571-581.
Lee, B., Sur, B., Shim, I., Lee, H. and Hahm, D.H. (2014). Baicalin improves chronic corticosterone-induced learning and memory deficits via the enhancement of impaired hippocampal brain-derived neurotrophic factor and cAMP response element-binding protein expression in the rat. Journal of Natural Medicines, 68(1): 132-143.
Li, C., Xing, G., Dong, M., Zhou, L., Li, J., Wang, G., et al. (2010). Beta-asarone protection against beta-amyloid-induced neurotoxicity in PC12 cells via JNK signaling and modulation of Bcl-2 family proteins. European Journal of Pharmacology, 635(1-3): 96-102.
Li, Z., Zhao, G., Qian, S., Yang, Z., Chen, X., Chen, J., et al. (2012). Cerebrovascular protection of beta-asarone in Alzheimer’s disease rats: a behavioral, cerebral blood flow, biochemical and genic study. Journal of Ethnopharmacology, 144(2): 305-312.
Lim, H.W., Kumar, H., Kim, B.W., More, S.V., Kim, I.W., Park, J.I., et al. (2014). β-Asarone (cis-2,4,5-trimethoxy-1-allyl phenyl), attenuates pro-inflammatory mediators by inhibiting NF-κB signaling and the JNK pathway in LPS activated BV-2 microglia cells. Food and Chemical Toxicology, 72(10): 265-272.
Liu, J., Li, C., Xing, G., Zhou, L., Dong, M., Geng, Y., et al. (2010). Beta-asarone attenuates neuronal apoptosis induced by Beta amyloid in rat hippocampus. Yakugaku Zasshi: Journal of the Pharmaceutical Society of Japan, 130(5): 737-746.
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