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PENGARUH PEMBERIAN DIET TINGGI LEMAK TERHADAP EKSPRESI SOD1, SOD2 dan P16 PADA JANTUNG TIKUS (Rattus novergicus)

RIASARI MARDANI, dr. Nur Arfian, Ph.D.; dr. Nungki Anggorowati, Ph.D, Sp.PA.

2022 | Tesis | MAGISTER ILMU BIOMEDIK

Latar belakang: Gagal ginjal akut (GGA) septik merupakan kondisi GGA yang terjadi simultan dengan sepsis, tanpa disertai penyebab GGA lain yang jelas. Kejadian GGA septik diketahui berhubungan dengan luaran mortalitas dan morbiditas yang tinggi. Beberapa faktor prediktor kejadian mortalitas telah diteliti sebelumnya, namun menunjukkan hasil inkonsisten, dan beberapa faktor belum pernah diteliti pada pasien anak. Tujuan: Menentukan GGA fase failure, kelebihan cairan, trombositopenia, abnormalitas kadar natrium, hiperkalemia, bikarbonat rendah, hipoalbuminemia, prokalsitonin tinggi, dan rasio neutrofil limfosit (RNL) tinggi sebagai faktor prediktor mortalitas pada anak dengan GGA septik. Metode: Dilakukan studi kohort retrospektif dengan subyek anak berusia 1 bulan- 18 tahun dengan GGA septik yang terindikasi perawatan intensif di RSUP Dr. Sardjito periode Januari 2017-September 2021 yang memenuhi kriteria inklusi dan eksklusi. Sampel diambil secara total sampling. Analisis bivariat untuk menghitung nilai p serta analisis multivariat dengan regresi logistik. Hubungan antar variabel dinyatakan dengan relative risk (RR) dan interval kepercayaan 95% dengan tingkat kemaknaan statistik p <0,05. Hasil: Seratus tiga puluh empat subyek dengan GGA septik diikutsertakan, dengan median usia 36 (8; 143,25) bulan. GGA diklasifikasikan sebagai fase risk (26,1%), injury (20,1%), dan failure (53,7%). Angka mortalitas sebesar 79,8%. Pada analisis multivariat didapatkan kelebihan cairan >10% (adjusted RR=5,653; IK95%=1,521-21,006; p=0,010) merupakan faktor prediktor independen kejadian mortalitas pada anak dengan GGA septik. Kesimpulan: Kelebihan cairan >10% merupakan faktor prediktor independen kejadian mortalitas pada anak dengan GGA septik, sedangkan kadar kalium <3,5 mmol/L merupakan faktor protektif terhadap mortalitas.

Introduction: Obesity is said to be a multifactorial disease, but environmental factors and habits, especially eating habits, have become the main factors in the increasing cases of obesity in the world when compared with genetic factors [1] According to [2] that giving a high-fat diet of more than 40% can cause hyperglycemia, hypertriglyceridemia, hyperleptinemia and obesity which pathophysiologically mimic obesity and metabolic syndrome in humans. Obesity is a condition associated with increased morbidity and mortality from chronic diseases and other health problems including cardiovascular disease [3]. Methods: The rats were acclimated for 7 days, and divide d into control group (C) and treatment groups, which induced HFD for 1 month (HF1), 2 month (HF2) and for 4 month (HF3). Each group consist of n=6. control group was given standard feed, AIN76A meanwhile the composisition feed from treatment group was 21.2% protein, 24% carbohydrates and 54.8% fat. Data collection of body weight and length of nasoanal to find out index Lee, level of cholesterol, trigliserida and glucose measured once a week and RNA isolation in heart tissue carried out et the end after sacrifice the rats. RT-PCR is used to determine the expression mrna sod1, sod2 and p16. Then, used immunohistochemical staining to see the localization of protein p16 in heart rats tissue. Result : data Lee index shows that there is significant difference between control and treatment group (p<0,05). however, the Lee index value of each group <300. so that the hfd-induced rats in this study were not obese. Profile lipid from the rats was induce HFD shows that there is difference significanHFy level of cholesterol and trigliseride between control and treatment groups (p<0,05). As well as on the glucose level. Expression mrna SOD1 and mrna SOD2 there is no difference significantly. Conclusion: Induction of a HFD might ascociate with senescence in the heart rats which affects expression p16.

Kata Kunci : diet tinggi lemak, jantung, SOD1, SOD2, P16, High Fat Diet, Obesitiy

  1. S2-2022-433386-abstract.pdf  
  2. S2-2022-433386-bibliography.pdf  
  3. S2-2022-433386-tableofcontent.pdf  
  4. S2-2022-433386-title.pdf