##plugins.themes.academic_pro.article.sidebar##

Download
pdf
Statistic
Read Counter : 82 Download : 53

##plugins.themes.academic_pro.article.main##

Abstract

The biology department's animal house at Iraq's AL-Qadisiyah University hosted this study. It's part of Iraq's AL-Qadisiyah University, to demonstrate that the Kidney and Liver were subjected to oxidative stress from reactive oxygen species, which led to harmful consequences of the indomethacin medication on molecular level. 40 male Wister rats, aged (2 -3) months, weighing between 200 and 300 grams. Four groups of 10 rats. Control, 5 mg/kg, 7 mg/kg, and 10 mg/kg of indomethacin were given for 21 days to the groups. After the experiment, the animals were killed by hanging. After twenty-one days ,each of the study groups that received indomethacin therapy saw a statistically significant reduction (P <0.0 5), which was a decrease in the amount of the cyp27b1 gene, with the level of decrease being largest in the group that received treatment with ten milligrams per kilogram for 21 days. There was no difference (p>< 0.05) in the expression of the FGF2 gene between individuals in the untreated group and those who were given 5 mg, 7 milligrams, while 10 mg/kg of indomethacin showed significant increase. In conclusion indomethacin cause decrease in the level of cyp27b1gene, and cause increase expression in FGF2 gene

Keywords

oxygen expression individuals untreated

##plugins.themes.academic_pro.article.details##

Creative Commons License

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

How to Cite
Noor Mahmood Majed Siraj. (2023). Evaluation of gene expression level of genes FGF2 and CYP27b1 in male Wister rats treated with indomethacin. Texas Journal of Medical Science, 21, 55–62. https://doi.org/10.62480/tjms.2023.vol21.pp55-62
Crossref
Scopus
Google Scholar
Europe PMC

References

  1. Abraham, C., Hart, J., Locke, S.M. and Baker, A.L., 2008. A case of indometacin-induced acute hepatitis developing into chronic autoimmune hepatitis. Nature clinical practice gastroenterology & hepatology, 5(3), pp.172-176.
  2. Argyrous, G. ed., 2009. Evidence for policy and decision-making: a practical guide. UNSW Press.
  3. Chena, W., Suruga, K., Nishimura, N., Gouda, T., Lam, V.N. and Yokogoshi, H., 2005. Comparative regulation of major enzymes in the bile acid biosynthesis pathway by cholesterol, cholate and taurine in mice and rats. Life Sciences, 77(7), pp.746-757.
  4. Choi YJ, Chakraborty S, Nguyen V, Nguyen C, Kim BK, Shim SI: Peritubular capillary loss is associated with chronic tubulointerstitial injury in human kidney: altered expression of vascular endothelial growth factor. Hum Pathol 2000; 31: 1491-1497
  5. Danielson, P.Á., 2002. The cytochrome P450 superfamily: biochemistry, evolution and drug metabolism in humans. Current drug metabolism, 3(6), pp.561-597.
  6. De Borst, M.H., Nauta, F.L., Vogt, L., Laverman, G.D., Gansevoort, R.T. and Navis, G., 2012. Indomethacin reduces glomerular and tubular damage markers but not renal inflammation in chronic kidney disease patients: a post-hoc analysis. PloS one, 7(5), p.e37957.
  7. Falzon, M., A. S. Milton, and M. D. Burke. "Are the decreases in hepatic cytochrome P-450 and other drug-metabolising enzymes caused by indomethacin in vivo mediated by intestinal bacterial endotoxins?: 16, 16-dimethylprostaglandin F2α prevents decreases in hepatic drug-metabolising enzymes due to exogenous endotoxin." Biochemical pharmacology 33, no. 8 (1984): 1285-1292.
  8. Falzon, M., Hogg, J., Milton, A.S. and Burke, M.D., 1984. Denaturation of hepatic microsomal cytochrome P-450 by non-steroidal anti-inflammatory drugs in vitro.
  9. Falzon, M., Whiting, P.H., Ewen, S.W., Milton, A.S. and Burke, M.D., 1985. Comparative effects of indomethacin on hepatic enzymes and histology and on serum indices of liver and kidney function in the rat. British journal of experimental pathology, 66(5), p.527.
  10. Imgrund, M., Gröne, E., Gröne, H.J., Kretzler, M., Holzman, L., Schlöndorff, D. and Rothenpieler, U.W., 1999. Re-expression of the developmental gene Pax-2 during experimental acute tubular necrosis in mice1. Kidney international, 56(4), pp.1423-1431.
  11. Katary, M.A. and Salahuddin, A., 2017. Gastroprotective effect of vanillin on indomethacin-induced gastric ulcer in rats: protective pathways and anti-Secretory mechanism. Clin Exp Pharmacol, 7(2), pp.2161-1459.
  12. LaFramboise, W.A., Bombach, K.L., Pogozelski, A.R., Cullen, R.F., Muha, N., Lyons-Weiler, J., Spear, S.J., Dhir, R.J., Guthrie, R.D. and Magovern, J.A., 2006. Hepatic gene expression response to acute indomethacin exposure. Molecular Diagnosis & Therapy, 10, pp.187-196.
  13. Lear, Stephanie, Silva, Patricio, Kelley, V.E. and Epstein, F.H., 1990. Prostaglandin E2 inhibits oxygen consumption in rabbit medullary thick ascending limb. American Journal of Physiology-Renal Physiology, 258(5), pp.F1372-F1378.
  14. Matsumoto, M., Makino, Y., Tanaka, T., Tanaka, H., Ishizaka, N., Noiri, E., Fujita, T. and Nangaku, M., 2003. Induction of renoprotective gene expression by cobalt ameliorates ischemic injury of the kidney in rats. Journal of the American Society of Nephrology, 14(7), pp.1825-1832.
  15. Mucha, K., Foroncewicz, B., Koziak, K., Czarkowska-Paczek, B. and Paczek, L., 2007. The effects of indomethacin on angiogenic factors mRNA expression in renal cortex of healthy rats. Journal of Physiology and Pharmacology, 58(1), p.165.
  16. Oliver, J.J., Rajapakse, N.W. and Evans, R.G., 2002. Effects of indomethacin on responses of regional kidney perfusion to vasoactive agents in rabbits. Clinical and experimental pharmacology and physiology, 29(10), pp.873-879.
  17. Patschan, D., Krupincza, K., Patschan, S., Zhang, Z., Hamby, C. and Goligorsky, M.S., 2006. Dynamics of mobilization and homing of endothelial progenitor cells after acute renal ischemia: modulation by ischemic preconditioning. American Journal of Physiology-Renal Physiology, 291(1), pp.F176-F185.
  18. Rainsford, K.D., Schweitzer, A. and Brune, K., 1981. Autoradiographic and biochemical observations on the distribution of non-steroid anti-inflammatory drugs. Archives Internationales de Pharmacodynamie et de Therapie, 250(2), pp.180-194.
  19. Rosenberger, C., Griethe, W., Gruber, G., Wiesener, M., Frei, U., Bachmann, S. and Eckardt, K.U., 2003. Cellular responses to hypoxia after renal segmental infarction. Kidney international, 64(3), pp.874-886.
  20. Schmittgen, T.D. and Livak, K.J., 2008. Analyzing real-time PCR data by the comparative CT method. Nature protocols, 3(6), pp.1101-1108.
  21. Sedrani, S.H. and El-Banna, A.A., 1987. Effect of indomethacin on plasma levels of vitamin D metabolites, oestradiol and progesterone in rabbits during early pregnancy. Comparative Biochemistry and physiology. A, Comparative Physiology, 87(3), pp.635-639.
  22. Sharfuddin, A.A. and Molitoris, B.A., 2011. Pathophysiology of ischemic acute kidney injury. Nature Reviews Nephrology, 7(4), pp.189-200.
  23. Silver, M.J. and Smith, J.B., 1975. Prostaglandins as intracellular messengers. Life Sciences, 16(11), pp.1635-1648.
  24. Tan, X.H., Zheng, X.M., Yu, L.X., He, J., Zhu, H.M., Ge, X.P., Ren, X.L., Ye, F.Q., Bellusci, S., Xiao, J. and Li, X.K., 2017. Fibroblast growth factor 2 protects against renal ischaemia/reperfusion injury by attenuating mitochondrial damage and proinflammatory signalling. Journal of cellular and molecular medicine, 21(11), pp.2909-2925.
  25. Trechsel, U., Taylor, C.M., Bonjour, J.P. and Fleisch, H., 1980. Influence of prostaglandins and of cyclic nucleotides on the metabolism of 25-hydroxyvitamin D3 in primary chick kidney cell culture. Biochemical and Biophysical Research Communications, 93(4), pp.1210-1216
  26. Vannay, Á., Fekete, A., Ádori, C., Tóth, T., Losonczy, G., László, L., Vásárhelyi, B., Tulassay, T. and Szabó, A., 2004. Divergence of renal vascular endothelial growth factor mRNA expression and protein level in post‐ischaemic rat kidneys. Experimental physiology, 89(4), pp.435-444.
  27. Villanueva, S., Céspedes, C. and Vio, C.P., 2006. Ischemic acute renal failure induces the expression of a wide range of nephrogenic proteins. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 290(4), pp.R861-R870.
  28. Villanueva, S., Cespedes, C., Gonzalez, A.A., Roessler, E. and Vio, C.P., 2008. Inhibition of bFGF-receptor type 2 increases kidney damage and suppresses nephrogenic protein expression after ischemic acute renal failure. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 294(3), pp.R819-R828.
  29. Wark, J.D., Larkins, R.G., Eisman, J.A. and Wilson, K.R., 1981. Regulation of 25-hydroxy-vitamin D-1 alpha-hydroxylase in chick isolated renal tubules: effects of prostaglandin E2, frusemide and acetylsalicylic acid. Clinical Science (London, England: 1979), 61(1), pp.53-59.
  30. Yamada, M., Matsumoto, T., Takahashi, N., Suda, T. and Ogata, E., 1983. Stimulatory effect of prostaglandin E2 on 1α, 25-dihydroxyvitamin D3 synthesis in rats. Biochemical Journal, 216(1), pp.237-240.
  31. Zhang, A., Cai, Y., Wang, P.F., Qu, J.N., Luo, Z.C., Chen, X.D., Huang, B., Liu, Y., Huang, W.Q., Wu, J. and Yin, Y.H., 2016. Diagnosis and prognosis of neutrophil gelatinase-associated lipocalin for acute kidney injury with sepsis: a systematic review and meta-analysis. Critical care, 20(1), pp.1-13.
  32. Zhu, X., Kong, Y., Huang, Y., Zhao, B. and Wang, J., 2019. Influence of strontium on vascular endothelial growth factor and fibroblast growth factor 2 expression in rat chondrocytes cultured in vitro. Biological trace element research, 190, pp.466-471.