Efek Neuroprotektif Vitamin D3 terhadap Jumlah Sel Purkinje Cerebellum yang Diinduksi Etanol

Abstract

Vitamin D₃ dapat bertindak sebagai antioksidan yang melindungi neuron terhadap kerusakan disebabkan stres oksidatif. Efek neurotoksik yang dimediasi oleh meningkatnya stress oksidatif dapat disebabkan oleh etanol. Otak kecil adalah salah satu daerah otak yang paling sensitif terhadap efek neurotoksik yang disebabkan oleh etanol. Penelitian ini bertujuan untuk mengetahui efek neuroprotektif vitamin D₃ untuk mencegah penurunan jumlah sel Purkinje cerebellum terhadap efek neurotoksik diinduksi etanol. Lima belas jantan galur Wistar (Rattus norvegicus) dibagi secara acak menjadi tiga kelompok. Kelompok kontrol diberi larutan garam normal, kelompok etanol diberi larutan etanol 20% dengan dosis 3  g / kg BB / hari dan vitamin D3 kelompok diberikan vitamin D3 1 pg / kg BB / hari dalam etanol 20% solusi dengan dosis 3 g / kg BB / hari, intraperitoneal. Setelah 30 hari perlakuan, tikus perfusi dan otak kecil itu dibedah untuk persiapan histologis. Pewarnaan histologi dengan violet cresyl dengan metode fractionator. Hasil penelitian menunjukkan jumlah sel Purkinje cerebellum kelompok etanol (744,552 ± 208.172,22)  lebih kecil dari kelompok kontrol (957,240 ± 160.353,03) dan vitamin D3 (983,448  ± 152.387,49) , tetapi secara statistik tidak berbeda bermakna (p> 0,05) jumlah sel Purkinje cerebellum antara ketiga kelompok. Disimpulkan bahwa vitamin D3 belum terbukti  memiliki efek neuroprotektif untuk mencegah penurunan jumlah sel Purkinje cerebellum disebabkan oleh pemberian etanol selama 30  hari.

Vitamin D₃ can act as an antioxidant that protects neurons against damage caused by oxidative stress. Neurotoxic effects that are mediated by increased oxidative stress can be induced by the ethanol. Cerebellum is one of the brain regions most sensitive to neurotoxic effects induced by the ethanol. The purpose of this study was to determine the neuroprotective effects of vitamin D₃ to prevent the decrease in the number of cerebellar Purkinje cells to the neurotoxic effects induced by ethanol. Fifteen male Wistar rats (Rattus norvegicus) were randomly divided into three groups. The control group was given normal saline solution; the ethanol group was given 20% ethanol solution at a dose of 3 g/kg BW/ day; and the vitamin D₃ group was given vitamin D₃ 1 µg/kg BW/day in 20% ethanol solution at a dose of 3 g/kg BW/day, intraperitoneally. After 30 day treatment, the rats were perfused and the cerebellum was dissected for histological preparations. Histological staining with cresyl violet was performed to assess the number of cerebellar Purkinje cells by the method of fractionator. The results showed the number of cerebellar Purkinje cells in the ethanol group (744.552 ± 208.172,22) was less than the control group (957.240 ± 160.353,03) and vitamin D₃ (983.448 ± 152.387,49) , but statistically not significant difference ( p>0.05) on the number of cerebellar Purkinje cells among the three groups. It can be concluded that vitamin D₃ had not been proven for its neuroprotective effect to prevent the decrease in the number of cerebellar Purkinje cells caused by ethanol administration for 30 days.