مطالعه اثرات محافظتی ویتامین E در برابر صدمات جنینی ایجادشده توسط لیپوپلی‌ساکارید‌ها در موش صحرایی
الموضوعات :
حسین محمدزاده
1
,
مسعود دل آشوب
2
,
منصور خاکپور
3
1 - دانش آموخته دانشکده دامپزشکی، واحد تبریز، دانشگاه آزاد اسلامی، تبریز، ایران.
2 - گروخ علوم پایه،دانشکده دامپزشکی،دانشگاه آزاد اسلامی،واحد تبریز،ایران
3 - گروه پاتوبیولوژی، واحد تبریز، دانشگاه آزاد اسلامی، تبریز، ایران.
تاريخ الإرسال : 27 السبت , ذو القعدة, 1438
تاريخ التأكيد : 04 الأربعاء , ربيع الأول, 1439
تاريخ الإصدار : 04 الأحد , جمادى الأولى, 1439
الکلمات المفتاحية:
ویتامین E,
آنتی‌اکسیدان,
موش صحرایی,
لیپوپلی‌ساکارید,
آسیب جنین,
ملخص المقالة :
لیپوپلی‌ساکارید ها از عوامل مهم آسیبهای جنین در طی مراحل رشد می‌باشند. این آسیب‌ها شامل تاخیر در رشد جنین، مرگ داخل رحمی جنین، جذب جنینی و زایمان زودرس بوده و با استرس اکسیداتیو ناشی از لیپوپلی‌ساکارید ها مرتبط می باشند. هدف از این مطالعه بررسی اثر محافظتی ویتامین E در برابر صدمات جنینی ناشی لیپوپلی‌ساکارید‌ها در موش صحرایی بود. در این مطالعه تعداد 48 سر موش صحرایی آبستن به 4 گروه تقسیم و به موش های گروه های 1 و 2 در روزهای 15 تا 17 آبستنی لیپوپلی‌ساکارید به میزان 75 میکروگرم بر کیلوگرم به صورت داخل صفاقی، به گروه های 2 و 3 یک هفته قبل از تجویز لیپوپلی‌ساکارید، ویتامین E روزانه به میزان 20 میلی گرم بر کیلوگرم به صورت داخل عضلانی و به گروه 4 به عنوان شاهد، سالین نرمال به صورت داخل صفاقی تزریق گردید. در روز 18 تمامی موش ها آسان کشی شدند. تعداد جنین‌های زنده و مرده شمارش شده، سپس تعداد جنین های زنده وزن گردیده و طول تاج-کفل در جنین های زنده و اسکلت در متاکارپ، متاتارس، بندهای انگشتان دست و پا و جناغ نیز اندازه گیری شد. میزان مالونیل دی آلدئید و گلوتاتیون بافتی کبد مادر، کبد جنین و جفت اندازه گیری شد. تجویز لیپوپلی‌ساکارید به طور معنی‌داری (05/0p<) موجب افزایش تلفات جنینی، کاهش وزن جنین و طول تاج-کفل در جنین های زنده و کاهش استخوانی شدن اسکلت در متاکارپ، متاتارس، بندهای انگشتان دست و پا و جناغ آن ها گردید. نتایج نشان داد که تجویز هم زمان ویتامین E و لیپوپلی‌ساکارید موجب کاهش آسیبهای ناشی از لیپوپلی‌ساکارید و بهبود صدمات مربوطه در جنین موش صحرایی می شود.
المصادر:
Aliverti, V., Bonanomi, L. and Giavini, E. (1979). The extent of fetal ossification as an index of delayed development in teratogenic studies on the rat. Teratology, 20(2): 237-242.
AlShamsi, M., Amin, A. and Adeghate, E. (2004). Beneficial effect of vitamin E on the metabolic parameters of diabetic rats. Cell Biochemistry, 261(1-2): 35-42.
Altavilla, D., Squadrito, G., Minutloi, L., Deodato, B., Bova, A., Sardella, A., et al. (1990). Inhibition of nuclear factor-kB activation by IRFI 042 protects against endotoxin-induced shock. Cardiovascular Research, 54(3): 684-693.
Bautista, A.P., Meszaros, K., Bojta, J. and Spitzer, J.J. (1990). Superoxide anion generation in the liver during the early stage of endotoxemia in rats. Journal of Leukocyte Biology, 48(2): 123-128.
Ben-Shaul, V., Lomnitski, A., Nyska, A., Zurovsky, Y., Bergman, M. and Grossman, S. (2001). The effect of natural antioxidants, NOA and apocynin, on oxidative stress in the rat heart following LPS challenge. Toxicology Letters, 123(1): 1-10.
Buhimschi, I.A., Buhimschi, C.S. and Weiner, C.P. (2003). Protective effect of N-acetylcysteine against fetal death and preterm labor induced by maternal inflammation. American Journal of Obstetrics and Gynecology, 188(1): 203-208.
Cederberg, J., Siman, C.M. and Eriksson, U.J. (2001). Combined treatment with Vitamin E and Vitamin C decreases oxidative stress and improves fetal outcome in experimental diabetic pregnancy. Pediatrics Research, 49(6): 755-762.
Chen, Y.H., Wang, G.P., Wang, H., Sun, M.F., Wei, L.Z., Wei, W., et al. (2005). Lipopolysaccharide treatment down regulates the expression of the pregnant X receptor, cyp3a11 and mdr1a genes in mouse placenta. Toxicology, 211(3): 242-252.
Delashoub, M., Banan Khojasteh, S.M. and Khodadadi, A. (2014). Protective Role of Vitamin A against Fetal Injuries Induced by Lipopolysaccharides.Annual Research and Review in Biology, 4(12): 1948-1957. [In Persian]
Ejima, K., Koji, W., Tsuruta, D., Nanri, H., Kashimura, M. and Ikeda, M. (2000). Induction of apoptosis in placentas of pregnant mice exposed to lipopolysaccharides possible involvement of Fas/Fas ligand system. Biology of Reproduction, 62(1): 178-185.
Fukui, H., Brauner, B., Bode, J.C. and Bode, C. (1991). Plasma endotoxin concentrations in patients with alcoholic and non-alcoholic liver disease: reevaluation with an improved chromogenic assay. Journal of Hepatology, 12(2): 162-169.
Gayle, D.A., Beloosesky, R., Desai, M., Amidi, F., Nunez, S.E., Ross, M.G., et al. (2004). Maternal LPS induces cytokines in the amniotic fluid and corticotropin releasing hormone in the fetal rat brain. American Journal of Physiology and Regulative Integrated Comparative Physiology, 286(6): 1024-1029.
Griffith, O.W. (1980). Determination of glutathione and glutathione disulfide using glutathione reductase and 2-vinylpyridine. Analytical Biochemistry, 106(1): 207-212.
Herrera, E. and Barbas, C. (2001). Vitamin E action, metabolism and perspectives. Journal of Physiology and Biochemistry, 57(2): 43-56.
Jacob, A.L., Goldberg, P.K., Bloom, N., Degenshein, G.A. and Kozinn, P.G. (1997). Endotoxin and bacteria in portal blood. Gastroenterology, 72(6): 1268-1270.
Kalender, S., Kalender, Y. and Yel, M. (2005). Doxorubin hepatotoxicity and hepatic free radical metabolism in rats.The effect of vitamin E and catechin. Toxicology, 1209(1):39-45.
Kaya, H., Sezik, M., Ozkaya, O., Dittrich, R., Siebzehnrubl, E., Wildt, L., et al. (2004). Lipid peroxidation at various estradiol concentrations in human circulation during ovarian stimulation with exogenous gonadotropins. Hormones and Metabolic Research, 36(10): 693-695.
Lowry, O.H., Rosebrough, N.J., Farr, A.L. and Randall, R.G. (1951). Protein measurement with the Folin phenol reagent. Journal of Biology and Chemistry, 193(1): 265-275.
Malmezat, T., Breuille, D., Capitan, P., Mirand, P. and Obled, C. (2000). Glutathione turnover is increased during the acute phase of sepsis in rats. Journal of Nutrition, 130(5): 1239-1246.
Nordberg, J. and Arner, E.S. (2001). Reactive oxygen species, antioxidants and the mammalian thioredoxin system. Free Radicals Biology, 31(11): 1287-1312.
Ogando, D.G., Paz, M. and Franchi, A.M. (2003). The functional role of increased production of nitric oxide in lipopolysaccharide induced embryonic resorption in mice. Reproduction, 125(1): 95-110.
Parra, T., de Arriba, G., Conejo, J.R., Cantero, M., Arribas, I., Rodríguez-Puyol, D., et al. (1998). Effect of vitamin E on cyclosporine nephrotoxicity. Transplantation, 66(10): 1325-1329.
Radi, R., Beckman, J.S., Bush, K.M. and Freeman, B.A. (1991). The cytotoxic potential of superoxide and nitric oxide. Journal of Biology and Chemistry, 266(7): 4244-4250.
Riedel, W. and Maulik, G. (1999).an integrated response of the central nervous system to oxidative stress. Molecular Cell Biochemistry, 196(1-2): 125-132.
Rivera, D.L., Olister, S.M., Liu, X., Thompson, J.H., Zhang, X.J., Pennline, K., et al. (1998). Interleukin-10 attenuates experimental fetal growth restriction and demise. FASEB Journal, 12(2): 189-197.
Romero, R., Roslansky, P., Oyarzun, E., Wan, M., Emamian, M., Novitsky, T.J., et al. (1988). Labor and infection. II. Bacterial endotoxin in amniotic fluid and its relationship to the onset of preterm labor. Labor and Infection, 158(5): 1044-1049.
Sabik, L.M.E. and Abdel-Rahman, S.S. (2009). Alpha-tocopherol and ginger are protective on Cyclophosphamide induced gonadal toxicity in adult male albino rats. Basic Applied Pathology, 2(1):9-21.
Savitha, S., Tamilselvan, J., Anusuyadevi, M. and Panneerselvam, C. (2005). Oxidative stress on mitochondrial antioxidant defense system in the aging process. Role of DL-a-lipoic acid and L-carnitine. Clinica Chimica Acta, 355(1-2): 173-180.
Silver, R.M., Edwin, S.S., Trautman, M.S., Simmons, D.L., Branch, D.W., Dudley, D.J., et al. (1995). Production of a newly recognized form of inducible cyclooxygenase (COX-2) in murine decidua in response to lipopolysaccharide. Journal of Clinical Investigation, 95(2): 725-731.
Shen, X., Sun, J. and Xie, LM. (2005). Effects of dietary supplementation with vitamin E and selenium on rat hepatic stellate cell apoptosis. World Journal of Gastroentrology, 28(32): 49-61.
Traber, M.G. and Atkinson, G. (2007). Vitamin E, antioxidant and nothing more. Free Radicals Biology and Medicine, 43(1): 4-15.
Tsiotou, A.G., Sakorafas, G.H., Anagnostopoulos, G. and Bramis, J. (2005). Septic shock current pathogenetic concept from a clinical perspective. Medical Science Monitoring, 11(3): 76-85.
Wasowicz, W., Neve, J. and Peretz, A. (1993). Importance of extraction pH and influence of sample preservation and storage. Clinical Chemistry, 39(12): 2522-2526.
Xu, D.X., Chen, Y.H., Wang, H., Zhao, L., Wang, G.P. and Wei, W. (2006). Tumor necrosis factor alpha partially contributes to lipopolysaccharide-induced intra-uterine fetal growth restriction and skeletal development retardation in mice. Toxicology Letters, 163(1): 20-29.
Xu, D.X., Chen, Y.H., Zhao, L., Wang, H. and Wei, W. (2006). Reactive oxygen species are involved in lipopolysaccharide-induced intrauterine growth restriction and skeletal development retardation in mice. Gynecology, 195(6): 1707-1714.
Yuan-Hua, C.H., De-Xiang, X., Lei, Z.H., Hua, W., Jian-Ping, W., Wei, W., et al. (2006), Ascorbic acid protects against lipopolysaccharide-induced intra-uterine fetal death and intra-uterine growth retardation in mice. Toxicology, 217(1): 39-45.
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Aliverti, V., Bonanomi, L. and Giavini, E. (1979). The extent of fetal ossification as an index of delayed development in teratogenic studies on the rat. Teratology, 20(2): 237-242.
AlShamsi, M., Amin, A. and Adeghate, E. (2004). Beneficial effect of vitamin E on the metabolic parameters of diabetic rats. Cell Biochemistry, 261(1-2): 35-42.
Altavilla, D., Squadrito, G., Minutloi, L., Deodato, B., Bova, A., Sardella, A., et al. (1990). Inhibition of nuclear factor-kB activation by IRFI 042 protects against endotoxin-induced shock. Cardiovascular Research, 54(3): 684-693.
Bautista, A.P., Meszaros, K., Bojta, J. and Spitzer, J.J. (1990). Superoxide anion generation in the liver during the early stage of endotoxemia in rats. Journal of Leukocyte Biology, 48(2): 123-128.
Ben-Shaul, V., Lomnitski, A., Nyska, A., Zurovsky, Y., Bergman, M. and Grossman, S. (2001). The effect of natural antioxidants, NOA and apocynin, on oxidative stress in the rat heart following LPS challenge. Toxicology Letters, 123(1): 1-10.
Buhimschi, I.A., Buhimschi, C.S. and Weiner, C.P. (2003). Protective effect of N-acetylcysteine against fetal death and preterm labor induced by maternal inflammation. American Journal of Obstetrics and Gynecology, 188(1): 203-208.
Cederberg, J., Siman, C.M. and Eriksson, U.J. (2001). Combined treatment with Vitamin E and Vitamin C decreases oxidative stress and improves fetal outcome in experimental diabetic pregnancy. Pediatrics Research, 49(6): 755-762.
Chen, Y.H., Wang, G.P., Wang, H., Sun, M.F., Wei, L.Z., Wei, W., et al. (2005). Lipopolysaccharide treatment down regulates the expression of the pregnant X receptor, cyp3a11 and mdr1a genes in mouse placenta. Toxicology, 211(3): 242-252.
Delashoub, M., Banan Khojasteh, S.M. and Khodadadi, A. (2014). Protective Role of Vitamin A against Fetal Injuries Induced by Lipopolysaccharides.Annual Research and Review in Biology, 4(12): 1948-1957. [In Persian]
Ejima, K., Koji, W., Tsuruta, D., Nanri, H., Kashimura, M. and Ikeda, M. (2000). Induction of apoptosis in placentas of pregnant mice exposed to lipopolysaccharides possible involvement of Fas/Fas ligand system. Biology of Reproduction, 62(1): 178-185.
Fukui, H., Brauner, B., Bode, J.C. and Bode, C. (1991). Plasma endotoxin concentrations in patients with alcoholic and non-alcoholic liver disease: reevaluation with an improved chromogenic assay. Journal of Hepatology, 12(2): 162-169.
Gayle, D.A., Beloosesky, R., Desai, M., Amidi, F., Nunez, S.E., Ross, M.G., et al. (2004). Maternal LPS induces cytokines in the amniotic fluid and corticotropin releasing hormone in the fetal rat brain. American Journal of Physiology and Regulative Integrated Comparative Physiology, 286(6): 1024-1029.
Griffith, O.W. (1980). Determination of glutathione and glutathione disulfide using glutathione reductase and 2-vinylpyridine. Analytical Biochemistry, 106(1): 207-212.
Herrera, E. and Barbas, C. (2001). Vitamin E action, metabolism and perspectives. Journal of Physiology and Biochemistry, 57(2): 43-56.
Jacob, A.L., Goldberg, P.K., Bloom, N., Degenshein, G.A. and Kozinn, P.G. (1997). Endotoxin and bacteria in portal blood. Gastroenterology, 72(6): 1268-1270.
Kalender, S., Kalender, Y. and Yel, M. (2005). Doxorubin hepatotoxicity and hepatic free radical metabolism in rats.The effect of vitamin E and catechin. Toxicology, 1209(1):39-45.
Kaya, H., Sezik, M., Ozkaya, O., Dittrich, R., Siebzehnrubl, E., Wildt, L., et al. (2004). Lipid peroxidation at various estradiol concentrations in human circulation during ovarian stimulation with exogenous gonadotropins. Hormones and Metabolic Research, 36(10): 693-695.
Lowry, O.H., Rosebrough, N.J., Farr, A.L. and Randall, R.G. (1951). Protein measurement with the Folin phenol reagent. Journal of Biology and Chemistry, 193(1): 265-275.
Malmezat, T., Breuille, D., Capitan, P., Mirand, P. and Obled, C. (2000). Glutathione turnover is increased during the acute phase of sepsis in rats. Journal of Nutrition, 130(5): 1239-1246.
Nordberg, J. and Arner, E.S. (2001). Reactive oxygen species, antioxidants and the mammalian thioredoxin system. Free Radicals Biology, 31(11): 1287-1312.
Ogando, D.G., Paz, M. and Franchi, A.M. (2003). The functional role of increased production of nitric oxide in lipopolysaccharide induced embryonic resorption in mice. Reproduction, 125(1): 95-110.
Parra, T., de Arriba, G., Conejo, J.R., Cantero, M., Arribas, I., Rodríguez-Puyol, D., et al. (1998). Effect of vitamin E on cyclosporine nephrotoxicity. Transplantation, 66(10): 1325-1329.
Radi, R., Beckman, J.S., Bush, K.M. and Freeman, B.A. (1991). The cytotoxic potential of superoxide and nitric oxide. Journal of Biology and Chemistry, 266(7): 4244-4250.
Riedel, W. and Maulik, G. (1999).an integrated response of the central nervous system to oxidative stress. Molecular Cell Biochemistry, 196(1-2): 125-132.
Rivera, D.L., Olister, S.M., Liu, X., Thompson, J.H., Zhang, X.J., Pennline, K., et al. (1998). Interleukin-10 attenuates experimental fetal growth restriction and demise. FASEB Journal, 12(2): 189-197.
Romero, R., Roslansky, P., Oyarzun, E., Wan, M., Emamian, M., Novitsky, T.J., et al. (1988). Labor and infection. II. Bacterial endotoxin in amniotic fluid and its relationship to the onset of preterm labor. Labor and Infection, 158(5): 1044-1049.
Sabik, L.M.E. and Abdel-Rahman, S.S. (2009). Alpha-tocopherol and ginger are protective on Cyclophosphamide induced gonadal toxicity in adult male albino rats. Basic Applied Pathology, 2(1):9-21.
Savitha, S., Tamilselvan, J., Anusuyadevi, M. and Panneerselvam, C. (2005). Oxidative stress on mitochondrial antioxidant defense system in the aging process. Role of DL-a-lipoic acid and L-carnitine. Clinica Chimica Acta, 355(1-2): 173-180.
Silver, R.M., Edwin, S.S., Trautman, M.S., Simmons, D.L., Branch, D.W., Dudley, D.J., et al. (1995). Production of a newly recognized form of inducible cyclooxygenase (COX-2) in murine decidua in response to lipopolysaccharide. Journal of Clinical Investigation, 95(2): 725-731.
Shen, X., Sun, J. and Xie, LM. (2005). Effects of dietary supplementation with vitamin E and selenium on rat hepatic stellate cell apoptosis. World Journal of Gastroentrology, 28(32): 49-61.
Traber, M.G. and Atkinson, G. (2007). Vitamin E, antioxidant and nothing more. Free Radicals Biology and Medicine, 43(1): 4-15.
Tsiotou, A.G., Sakorafas, G.H., Anagnostopoulos, G. and Bramis, J. (2005). Septic shock current pathogenetic concept from a clinical perspective. Medical Science Monitoring, 11(3): 76-85.
Wasowicz, W., Neve, J. and Peretz, A. (1993). Importance of extraction pH and influence of sample preservation and storage. Clinical Chemistry, 39(12): 2522-2526.
Xu, D.X., Chen, Y.H., Wang, H., Zhao, L., Wang, G.P. and Wei, W. (2006). Tumor necrosis factor alpha partially contributes to lipopolysaccharide-induced intra-uterine fetal growth restriction and skeletal development retardation in mice. Toxicology Letters, 163(1): 20-29.
Xu, D.X., Chen, Y.H., Zhao, L., Wang, H. and Wei, W. (2006). Reactive oxygen species are involved in lipopolysaccharide-induced intrauterine growth restriction and skeletal development retardation in mice. Gynecology, 195(6): 1707-1714.
Yuan-Hua, C.H., De-Xiang, X., Lei, Z.H., Hua, W., Jian-Ping, W., Wei, W., et al. (2006), Ascorbic acid protects against lipopolysaccharide-induced intra-uterine fetal death and intra-uterine growth retardation in mice. Toxicology, 217(1): 39-45.
