Pengaruh Pemberian Vitamin D3 Terhadap Kadar Reactive Oxygen Species (ROS) pada Sel PHM1-41 yang Mengalami Hipoksia

Muhammad Alamsyah Aziz, Sofie Rifayani Krisnadi, Budi Setiabudiawan, Budi Handono

Abstract


Kelahiran preterm (kurang bulan) merupakan salah satu penyebab kematian bayi yang hingga kini menjadi permasalahan di seluruh dunia. Salah satu mekanisme patofisiologis yang menyebabkan kelahiran kurang bulan adalah aktivitas sumbu hipotalamus-pituitari-adrenal (HPA) pada ibu dan janin. Stres maternal biologis berupa hipoksia merupakan salah satu penyebab terjadi mekanisme kelahiran kurang bulan melalui jalur aktivasi sumbu HPA ibu dan sebagai respons terhadap reactive oxygen species (ROS).  Vitamin D3 sebagai salah satu sumber ion Ca2+ dibutuhkan untuk mekanisme kontraksi dan relaksasi otot halus miometrium. Selain itu, vitamin D diduga berpengaruh terhadap kerja sumbu HPA. Tujuan penelitian ini adalah mengetahui pengaruh penambahan vitamin D3 pada sel lini PHM1-41 yang menjadi model in vitro dari kontraksi miometrium pada ibu hamil yang mengalami stres hipoksia terhadap kadar ROS intraseluler sel PHM1-41. Penelitian dilakukan di Laboratorium penelitian Aretha Medika Utama, Biomolecular and Biomedical Research Centre dengan kurun waktu penelitian dari bulan Desember 2017 hingga Februari 2018. Sel PHM1-41 yang telah dikultur dengan keadaan hipoksia selama 24 jam diberi penambahan vitamin D3, kemudian diukur kadar ROS intraselulernya. Hasil menunjukkan bahwa kadar ROS menurun signifikan pada kelompok sel yang diberi penambahan vitamin D3 dengan konsentrasi 150 nM dibanding dengan kelompok sel kontrol hipoksia. Hal ini menunjukkan  bahwa penambahan vitamin D3 150 nM memiliki potensi mencegah kelahiran kurang  bulan

Effects of Vitamin D3 Treatment on Reactive Oxygen Species (ROS) Level in PHM1-41 Cell Line Experiencing Hypoxia

Preterm birth is one of the major global cause of perinatal mortality. One of the pathophysiologic mechanisms leading to preterm birth is the Hypothalamic-Pituitary-Adrenal (HPA) axis activity of mother and fetus.. Maternal biological stress, such as hypoxia condition, is one of the trigger  of preterm birth through the activation of HPA axis as a response to the reactive oxygen species (ROS). Vitamin D3 as a source of Ca2+ ion is needed for myometrium smooth muscle’s contraction and relaxation mechanism. Vitamin D is also thought to strongly influence the HPA axis’s work. The purpose of this study was to determine the effect of  vitamin D3 provisionon PHM1-41 cell line induced by hypoxia as an  of pregnant women’s myometrium contraction through assessment of intracellular ROS level in PHM1-41 cell lines. This study was conducted in Aretha Medika Utama Biomolecular and Biomedical Research Centre from December 2017 to February 2018. PHM1-41 cells were cultured for 24 hours in hypoxia condition,Vitamin D3 was then added and the level of intracellular ROS was measured. Results showed that the ROS level decreased in cell clusters receiving 150nM vitamin D3 when compared to control hypoxia cell cluster. This indicates that the provision of 150nM vitamin D3 potentially prevents preterm  labor incidents.  


Keywords


Vitamin D3;Kadar ROS; Sel PHM1-41; Hipoksia

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References


WHO. Born too soon: The global action report on preterm birth. Report November 2012. Geneva: WHO News Preterm Birth Report; 2012.

Blencowe H, Cousens S, Oestergaard M, Chou D, Moller AB, Narwal R, dkk. National, regional and worldwide estimates of birth. Lancet. 2012;379(9832):2162–72.

Lockwood C, Kuczynski E. Makers of risk for delivery. J PerinMed. 1999;27:5-20.

Goldenberg RL, Culhane JF, Iamss JD, Romero R. Epidemiology and cause of birth. Lancet. 2008;371:75–84.

Villar J, Papageorghiou AT, Knight HE, Gravett MG, Iams J, Waller SA. The preterm birth syndrome: a prototype phenotypic classification. Am J Obstet Gynecol. 2012; 206(2):119–23.

Burthon GJ, Jauniaux E. Oxidative stress, best practice and research. Clin Obstet Gynaecol. 2010;25:287–99.

Jereme GS, Chen HJC, Semia C, Lavidis NA. Activation of hipotalamus-pituitary-adrenal stress axis induces cellular oxidative stress. Frontiers Neurosci. 2015;8(456):1–6.

Gomes DS, Machado NR, Fernandes JRM. Cell signaling through protein kinase C oxidation and activation. Int J Mol Sci. 2012;13(9): 10697–721.

Moroz LA, Simhan HN. Rate of sonographic cervical shortening and biologic pathwya of spontaneous preterm birth. Am J Obstet Gynecol. 2014;210(6):555.e1-5.

Kramer MS, Lydon J, Seguin L, Goulet L, Khan SR, McNamara H, dkk. Stress pathway to spontaneous preterm birth: The role of stressors, physcological distress, and stress hormones. Am J Epidemiol. 2009;169(11):1319–26.

Thota C, Laknaur A, Farmer T, Lason G, Al-hendy A, Ismail N. Vitamin D regulates contractile profile in human uterine myometrial cells via NFkB pathway. Am J Obstet Gynecol. 2014;210(4):347.e1-347.e10.

Dutta EH, Faranak B, Boldogh I, Saade GR, Taylor BD, Kacerovsky M, Menon R. Oxidative stress damage-associated molecular signaling pathway differentiate spontaneous preterm birth and preterm premature rupture of the membran. Mol Hum Reprod. 2016;22(2):143–57.

Burthon GJ, Jauniaux E. Oxidative stress, best practice and research. Clin Obstet Gynaecol. 2010;25:287–99.

Bodnar LM, Simhan HN. Vitamin D maybe link to black white disparties in adverses birth outcomes. Obstet Gynecol Surv. 2010;65(4):273–84.

Christakos S, Ajibade DV, Dhawan P, Fechner AJ, Mady LJ. Vitamin D: metabolism. Metab Clin North Am. 2010;39(2):243–53.

Wong SM, Delansorne R, Man RY, Syenningsen P, Vanhoutte PM. Chronic treatment with vitamin D lowers arterial blood pressure and reduce endothelium dependent contraction in the aorta of the spontaneously hypertensive rat. Am J Physiol Heart Physiol. 2010;299(4):1226–34.

De-Regil LM, Palacios C, Ansary A, Kulier R, Peña-Rosas JP. Vitamin D supplementation for women during pregnancy. Cochrane Database Syst Rev. 2012;(2):CD008873

Ginde AA, Sullivan AF, Mansbach JM, Camargo CA. Vitamin D insufficiency in pregnant and nonpregnant women of childbearing age in the United States. Am J Obstet Gynecol. 2010;202(5):436.e1–8.




DOI: http://dx.doi.org/10.15395/mkb.v50n3.1408

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