PERUBAHAN EKSPRESI MCP-1 DAN JUMLAH MAKROFAG PADA PERIODE AKUT DAN KRONIS MODEL CEDERA ISKEMIA/REPERFUSI GINJAL MENCIT

DWINA AGRILA LAKABELA, dr. Nur Arfian, Ph.D; dr. Dian Prasetyo W., M.Sc; dr. Widya Wasityastuti, M.Sc., M.Med.Ed., Ph.D

2017 | Skripsi | S1 PENDIDIKAN DOKTER

Latar Belakang: Salah satu penyebab utama cedera ginjal akut adalah cedera iskemia/reperfusi. Dalam hal ini, respon inflamasi memiliki peranan yang sangat penting terkait patofisiologi cedera ginjal akut. Inflamasi diinisiasi oleh mediator inflamasi yang dilepaskan karena adanya disfungsi endolel, salah satu mediator inflamasi yang diketahui adalah MCP-1. Inflamasi juga ditandai dengan adanya infiltrasi makrofag pada sel tubulus ginjal yang mengalami cedera. Tujuan: Mengetahui bagaimana perubahan ekspresi MCP-1 dan jumlah makrofag pada periode akut dan kronis model cedera iskemia/reperfusi ginjal mencit. Metode: Subjek yang diteliti sebanyak 15 ekor mencit galur Swiss jantan usia 3-4 bulan dengan berat badan 30-40 gram, dibagi menjadi 3 kelompok, yaitu kelompok Sham Operation (SO, n=5), IR1 (n=5) dan IR12 (n=5). Model cedera iskemia/reperfusi dilakukan dengan menjepit hilus renalis kanan dan kiri ginjal mencit selama 30 menit. Ekspresi MCP-1 diperiksa dengan melihat densitas pita hasil elektroforesis, kemudian dianalisis dengan software ImageJ. Jumlah makrofag dilihat dengan menghitung jumlah sel yang terwarnai cokelat dengan perwarnaan imunohistokimia menggunakan antibodi anti CD68. Hasil: Cedera iskemia/reperfusi menyebabkan terjadinya peningkatan ekspresi MCP-1, dengan adanya perbedaan yang bermakna antara kelompok SO, IR1 dan IR12 (p<0,05 vs SO). Terdapat peningkatan jumlah makrofag dan perbedaan yang bermakna antara kelompok SO, IR1 dan IR12 (p<0,05 vs SO). Kesimpulan: cedera iskemia/reperfusi menyebabkan peningkatan ekspresi MCP-1 dan jumlah makrofag. Kata Kunci: cedera iskemia/reperfusi, MCP-1, jumlah makrofag, CD68

Background: One of the main causes of acute kidney injury is an ischemia/reperfusion injury. In this case, the inflammatory response has a very important role related to the pathophysiology of acute kidney injury. Inflammation is initiated by the inflammatory mediators that are released for their endolel dysfunction, one of the inflammatory mediators is MCP-1. Inflammation is also indicated by the infiltration of macrophages in injured renal tubular cells. Objective: To determine how the change of MCP-1 expression and macrophage numbers on the acute and chronic period model of kidney ischemia/reperfusion injury in mice. Methods: There were 15 male Swiss mice age 3-4 months and weighing 30-40 grams which were studied. Those mice were divided into three groups, namely Sham Operation (SO, n = 5), IR1 (n = 5) and IR12 (n = 5). Model of ischemia / reperfusion injury was done by clamping the right and left renal hilum of the mice's kidneys for 30 minutes. The expression of MCP-1 was checked by band density in electrophoresis, then analyzed with ImageJ software. The numbers of macrophages were seen by counting the number of cells which coloured brown by the immunohistochemistry staining using anti-CD68 antibody. Results: The ischemia / reperfusion injury leads to an increase of MCP-1 expression, along with significant difference between the groups of SO, IR1 and IR12 (p <0.05 vs SO). There was an increase in the number of macrophages and significant differences between the groups of SO, IR1 and IR12 (p <0.05 vs SO). Conclusion: ischemia / reperfusion injury caused an increased of MCP-1 expression and the number of macrophages. Keywords: ischemia/reperfusion injury, MCP-1, the number of macrophages, CD68

Kata Kunci : cedera iskemia/reperfusi, MCP-1, jumlah makrofag, CD68