EFEK HEPAPROTEKTIF GULA AREN TERHADAP KARBON TETRAKLORIDA PADA TIKUS

Abstract

Abstrak

 

Studi ini meneliti efek gula aren, senyawa bioaktif yang diisolasi dari gula aren, terhadap kerusakan hati akibat karbon tetraklorida (CCl₄). Tikus diperlakukan secara intraperitoneal dengan 0,5 ml / kg CCl₄ dan kelompok hewan yang berbeda menerima 25, 50, 100, dan 200 mg / kg sudar palem. Pada 24 jam setelah perawatan CCl₄, kadar aminotransferase serum dan peroksidasi lipid meningkat secara signifikan, sedangkan kadar glutathione hati menurun. Perubahan ini dilemahkan oleh gula aren. Studi histologis menunjukkan bahwa gula aren menghambat peradangan portal, nekrosis sentrizonal, dan hiperplasia sel Kupffer, yang merupakan tiga karakteristik paling umum dari kerusakan hati yang diinduksi CCl₄. Tingkat serum dan mRNA ekspresi tumor necrosis factor-α secara nyata meningkat dengan pengobatan CCl₄ tetapi ditekan oleh gula aren. Level mRNA dan ekspresi protein diinduksi nitric oxide synthase dan heme oksigenase-1 meningkat secara signifikan pada 24 jam setelah perawatan CCl₄. Gula aren melemahkan peningkatan protein dan ekspresi gen diinduksi nitric oxide synthase tetapi menambah peningkatan heme oxygenase-1. Temuan ini menunjukkan bahwa gula aren melindungi hepatosit dari kerusakan oksidatif yang disebabkan oleh CCl₄, dan perlindungan ini kemungkinan disebabkan oleh induksi ekspresi HO-1 dan penghambatan mediator proinflamasi.

 

Abstract

 

This study examined the effects of palm sugar, a bioactive compounds isolated from palm sugar, on carbon tetrachloride (CCl₄)-induced liver injury. Mice were treated intraperitoneally with 0.5 ml/kg CCl4 and different groups of animals received 25, 50, 100, and 200 mg/kg palm sudar. At 24 h after the CCl4 treatment, the level of serum aminotransferases and lipid peroxidation was significantly elevated, whereas the hepatic glutathione content was decreased. These changes were attenuated by palm sugar. The histological studies showed that palm sugar inhibited the portal inflammation, centrizonal necrosis, and Kupffer cell hyperplasia, which are the three most common characteristics of CCl₄-induced liver damage. The serum level and mRNA expression of tumor necrosis factor-α were markedly increased by the CCl₄ treatment but suppressed by palm sugar. The mRNA and protein expression levels of inducible nitric oxide synthase and heme oxygenase-1 increased significantly at 24 h after the CCl₄ treatment. Palm sugar attenuated the increase in the protein and gene expression of inducible nitric oxide synthase but augmented the increase in those of heme oxygenase-1. These findings suggest that palm sugar protects hepatocytes from the oxidative damage caused by CCl₄, and this protection is likely due to the induction of HO-1 expression and the inhibition of the proinflammatory mediators.