مطالعه اثرات محافظتی ویتامین E در برابر صدمات جنینی ایجادشده توسط لیپوپلی‌ساکارید‌ها در موش صحرایی
محورهای موضوعی :
آسیب شناسی درمانگاهی دامپزشکی
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.
تاریخ دریافت : 1396/05/28
تاریخ پذیرش : 1396/09/01
تاریخ انتشار : 1396/11/01
کلید واژه:
ویتامین E,
آنتی‌اکسیدان,
موش صحرایی,
لیپوپلی‌ساکارید,
آسیب جنین,
چکیده مقاله :
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.
چکیده انگلیسی:
Lipopolysaccharides (LPS) are one of the most important factors in the formation of embryonic damages. These damages include intra-uterine growth retardation, intra-uterine fetal death, embryonic absorption and preterm birth and are associated with oxidative stress caused by lipopolysaccharides. This study aimed to investigate the protective effect of vitamin E on lipopolysaccharide induced fetal damages in the rat. In this study, 48 pregnant rats were selected and allocated to 4 groups. In groups 1 and 2, 75 µgr/kg of lipopolysaccharides were injected intraperitoneally on day 15 to 17 of pregnancy. A week before administration of lipopolysaccharides to rats of groups 2 and 3, they received 20 mg/kg of intramuscular vitamin E daily. Group 4 received normal saline intraperitoneally as a control group. In day 18 of pregnancy all mice were euthanized. In each animal, the number of live and dead embryos were counted. Then the live fetuses were weighed and the length of crown–rump, metacarpus, metatarsus, anterior phalanges, posterior phalanges and sternum were determined. In addition, the amounts of malondialdehyde and glutathione were measured in maternal and embryonic liver and placenta. Administration of lipopolysaccharides significantly increased fetal mortality and reduced fetal weight, length of the tail and crown–rump, live embryos and skeletal ossification of the metacarpus, metatarsus, anterior and posterior phalanges and sternum. Results showed that simultaneous administration of vitamin E and lipopolysaccharides reduced damages and improved respective injuries in mice embryos.
منابع و مأخذ:
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.
