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Abstrak :
Telah dilakukan uji sitotoksik metabolit sekunder kapang endofit 1.2.11 tanaman Bruce javanica (L) merr.

Abstrak :
Telah dilakukan uji sitotoksik metabolit sekunder kapang endofit 1.2.11 tanaman Brucea javanica (L. ) Merr. Sampel tanaman diambil dari Cianjur, bagian tanaman yang digunakan adalah buah. Uji sitotoksik dilakukan terhadap sel Ruji, NS-l, sel HeLa dan sel Vero. Pengamatan dilakukan selama 24 jam dan 48 jam dengan menghitung sel ludup menggunakan metode tripan biru. Penghitungan l CM dilakukan secara aritmatikal dengan rumus Ricd and Muench. Untuk melihat mekanisme kerja pada proses sitotoksik dilakukan teknik pengecatan DNA menggunakan etidium bromida dan acridine orange. Dari penelitian ini diperoleh lCft) terhadap sel Raji 58,35 fjg/ml, 88,39yg/ml; IC50sel NS-1 162,09 pg/ml, 66,24 p. g/ml; IC^ sel HeLa 361,21 pg/ml, 219,97 pg/ml. IC^sel Vero 1075.18 ug/ml, 656,82 ng/ml. Pengamatan dilakukan dalam waktu 24 jam dan 48 jam. Mekanisme kerja dari metabolit sekunder kapang endofit 1.2. 11 terhadap sel NS-1 cenderung melalui mekanisme apoptosis. (Med J Indones 2006; 15:137-44)

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Cytotoxic assay of secondary metabolite endophytic fungus 1.2.11 from Brucea javanica (L.) Merr has been carried out. Brucea Javanica fruit collected from Cianjur was used in this experiment. Cytotoxic assay was done on Raji, NS-1, HeLa and Vero cells. The observation was done for 24 hours and also for 48 hours. I CM was calculated using the Rich and Muench theory. To observe the working mechanism ofcytotoxic process, DNA staining with etidium bromide and acridine orange was conducted. The cytotoxic assay of endophytic fungi 1.2.11 showed an ICft) of 58.35p.g/ml, 88.39 pg/ml on Raji ceil; 162.09 pg/ml, 66.24 pg/ml on NS cell; 361.21 fjg/ml, 219.97 fjg/ml on HelM cell; and lastly 1075.18 fjg/ml, 656.82 /jg/ml on Vero cell after 24 and 48 hour incubation respectively. The results of this study showed that secondary metabolite of endophytic fungus 1.2.11 has selective cytotoxic effect towards cancer cell and also showed that it might cause apoptosis in NS-1 cell. (Med J Indones 2006; 15:137-44)

Abstrak :
Pada penelitian ini, asam risinoleat diesterifikasi dengan dry metanol dan katalis KOH dengan sistem reflux. Metil risinoleat yang terbentuk dioksidasi pada ikatan rangkapnya membentuk diol menggunakan KMnO4 encer dalam suasana basa pada suhu 0oC. Metil risinoleat kemudian diamidasi menggunakan asam amino glisin dan asam amino fenilalanin untuk menghasilkan senyawa lipoamida. Hasil karakterisasi lipoamida yang terbentuk menggunakan FTIR menunjukkan adanya pita serapan ulur N-H dan O-H yang overlaping pada bilangan gelombang 3445,47 cm-1 untuk lipoamida glisin-risinoleat dan 3434,06 cm-1 untuk lipoamida fenilalanin-risinoleat. Selain itu, muncul puncak serapan medium vibrasi C-N pada bilangan gelombang 1217,90 cm-1 pada lipoamida glisin-risinoleat dan 1217,59 cm-1 pada lipoamida fenilalanin-risinoleat. Hal ini menunjukkan ikatan amida yang terbentuk dari proses amidasi. Hasil uji sitotoksik MTT senyawa lipoamida terhadap sel HeLa menunjukkan bahwa nilai IC50 lipoamida glisin-risinoleat sebesar 120 µg/mL yang termasuk ke dalam kategori cukup aktif, sedangkan IC50 lipoamida fenilalanin-risinoleat sebesar 250 µg/mL yang tergolong memiliki sifat sitotoksisitas yang lemah terhadap sel HeLa. ......In this study, ricinoleic acid from castor oil was esterified with dry methanol and KOH catalyst using the reflux system. The methyl ricinoleate formed was oxidized on its double bonds to form a diol using dilute KMnO4 under alkaline conditions at 0oC. Methyl ricinoleate was then reacted through amidation process using amino acid glycine and amino acid phenylalanine to produce lipoamides. The results of characterization of lipoamides formed using FTIR showed that there were overlapping N-H and O-H stretch bands at wave numbers 3445.47 cm-1 for glycine-ricinoleate lipoamide and 3434.06 cm-1 for phenylalanine-ricinoleate lipoamide. In addition, the medium absorption peak of C-N appeared at the wave number 1217.90 cm-1 for glycine-ricinoleate lipoamide and 1217.59 cm-1 for phenylalanine-ricinoleate lipoamide. These showed that the amide bonds were formed from the amidation process. The results of the MTT cytotoxic assay of lipoamide compounds against HeLa cells showed that the IC50 value of glycine-ricinoleate lipoamide was 120 µg / mL which was considered quite active, while the IC50 value of phenylalanine-ricinoleate lipoamide was 250 µg / mL which was classified as having weak cytotoxicity properties against HeLa cells