Atherosclerosis is still a major health problem, because 20% of death in the world is caused by atherosclerosis diseases like stroke and myocardial infarct. One of animal models that was successful in atherosclerosis research was New Zealand white rabbit. The purpose of this preliminary research was to determine the atherogenic diet of white rats (Rattus novergicus strain Wistar) as animal model of atherosclerosis especially to find fixed composition and time of the atherogenic diet taken.This research used male; 2 months age, 150-200 grams body weight of white rats Rattus novergicus strain Wistar. The rats were divided into 5 groups in equal number, 4 rats respectively. They were a negative control group without diet treatment and 4 groups as treatment groups which were given hipercholesterol diet. Atherogenic diet composed of PARS , wheat flour, cholesterol, cholic acid, pork oil and water. Data were obtained by measuring of blood cholesterol level and foam cell formation. The result showed, the atherogenic diet inducing foam cell formation and hypercholesterolemia of these rats were mixtures of PARS , wheat flour and 2% cholesterol, 0,2% cholic acid, 10% pork oil given for 8 weeks. It can be concluded, that white rats Rattus novergicus strain Wistar could be used as animal model for atherosclerotic research, by giving them the atherogenic diet for 8 weeks.
In acute infection, malaria will induce cellular immunity by activating T lymphocytes and macrophages cells. This induction indirectly triggers free radicals production in order to eliminate the parasites from red blood cells, however high concentration of thismolecules can cause vital tissue pathological changes on host. In late phase of malarial infection, there are immunosupression on macrophages activity including antigen presenting and secretion of immunoregulated mediator. It has been anticipated, vitamin C as antioxidant would diminish the side effect of thesefree radicals during malarial infection and increase the immunity. To see the effect of combination chloroquin and vitamin C in hastening the recuperative process by decreasing parasitemia and increasing the phagocytosis function of macrofages during Plasmodium berghei infection. This study has been carried out using 3 groups of BALB/c mice, all group were inoculated with 1x107Plasmodium berghei infected red-blood cells. No drug was given on control group (IK). In experimental group we introduced an oral therapy ofchloroquin for 5 days in 1.4 mg/cc dosage and vitamin C for 7 days in 0.2 mg/cc dosages concurrently with a Plasmodium berghei inoculation (IKC). One group was only given chloroquin at the same dosage and no drug was given at the control group (IK).
Penelitian ini bertujuan untuk mengetahui pengaruh suplemen L-arginin subakut peroral pada tikus diabetesstreptozotosin terhadap respons kontraksi aorta melalui mekanisme pencegahan peningkatan stress oksidatif. Larginine diberikan selama 8 minggu pada tikus diabetes dengan dosis 10, 100 dan 1000 mg.kg-1 BB.hari-1. Parameter yang diukur adalah MDA-plasma untuk menilai oksidatif stress dan teknik bioassay dengan isolasi organ terpisah aorta ring untuk menilai respons reseptor adrenergik- 1 di otot polos aorta terhadap fenilefrin (PE). Dari respons kontraksi aorta dapat diketahui nilai Emaks dan pD 2 PE. Hasil penelitian menunjukkan bahwa pemberian L-arginin 100, 1000 mg.kg-1 BB.hari-1 pada tikus diabetes dapat mencegah peningkatan MDA-plasma (p<0.001). Pemberian L-arginin dosis 100, 1000 mg.kg-1 BB.hari-1 dapat mencegah peningkatan respons kontraksi aorta terhadap PE melalui pencegahan peningkatan Emaks (p<0.000) dan menurunkan pD 2 pada dosis 1000 mg.kg-1 BB.hari-1 (p<0.001). Hasil Jalur Hubungan menunjukkan pencegahan peningkatan Emaks melalui jalur pencegahan peningkatan MDA (p<0.012) dan penurunan pD 2 melalui jalur langsung (p<0.016). Berdasarkan haasil penelitian dapat disimpulkan bahwa pemberian suplemen Larginin pada tikus diabetes dapat mencegah peningkatan respons kontraksi aorta terhadap PE dengan cara: (1) mencegah peningkatan Emaks melalui pencegahan peningkatan MDA (jalur tidak langsung); dan (2) secara langsung menurunkan afinitas reseptor adrenergik- 1 .
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