Sains
Malaysiana 38(5)(2009): 761–766
Infeksi Plasmodium berghei dan
Kesannya ke atas Pengisyaratan MAP Kinase
Eritrosit Perumah
(Plasmodium
berghei Infection and its Effect on MAP Kinase Signaling in its Erythrocyte Host)
Mohd Fakharul Zaman Raja Yahya
Pusat Pengajian Bioperubatan
& Kesihatan
Kolej Universiti Kejururawatan
& Kesihatan Masterskill
43200 Cheras, Selangor Darul
Ehsan, Malaysia
Hasidah Mohd Sidek*
Pusat Pengajian Biosains &
Bioteknologi
Fakulti Sains & Teknologi,
Universiti Kebangsaan Malaysia
43600 UKM Bangi, Selangor Darul Ehsan,
Malaysia
Diserahkan: 24 Jun 2008 / Diterima:
12 Mac 2009
ABSTRAK
Kajian ini melibatkan pemantauan perkembangan parasitemia dan
taburan morfologi Plasmodium berghei sewaktu
infeksi parasit dalam mencit, serta penentuan kesan infeksi P. berghei ke
atas pengisyaratan MAP kinase
eritrosit perumah. Analisis mikroskop ke atas slaid calitan darah terwarna-Giemsa yang
disediakan daripada mencit terinfeksi-P. berghei (strain PZZ1/00) menunjukkan darjah parasitemia mencapai sehingga 70% dalam
masa dua minggu selepas penyuntikan parasit. Morfologi
cecincin dan trofozoit parasit dicerap dengan jelas sepanjang tempoh infeksi
manakala morfologi skizon parasit hanya dicerap dengan ketara selepas hari
ketiga selepas penyuntikan parasit. Pemblotan Western [antibodi primer:
anti-MAP kinase (ERK-1/2 tak terfosfat) monoklon; antibodi sekunder: anti-IgG,
poliklon terkonjugat-HRP] ke atas
protein sitosol eritrosit terinfeksi-P. berghei (70%
parasitemia) susulan pemisahan SDS-PAGE menunjukkan bahawa keamatan protein imunoreaktif-MAP kinase eritrosit berberat molekul 42 dan 44 kDa didapati
meningkat secara signifikan (p<0.05) pada 70% iaitu peningkatan sebanyak
21.5% dan 22.3% masing-masing berbanding sampel kawalan tanpa infeksi. Samada kesan infeksi P. berghei (70%
parasitemia) ke atas pengisyaratan MAP kinase perumah ini berkaitan dengan pengaktifan enzim
ini perlu dikaji dengan lebih lanjut.
Kata kunci: MAP kinase; malaria; Plasmodium berghei; transduksi isyarat
ABSTRACT
The present
investigation involves monitoring the development of parasitemia and the
distribution of Plasmodium berghei morphologies
during parasite infection in mice as well as the effect P. berghei infection
on MAP kinase signaling in its
erythrocyte host. Microscopic analyses of Giemsa-stained blood films prepared
from P. berghei (strain PZZ1/00)-infected mice showed that the level of parasitemia reached
up to 70% two weeks after inoculation of the parasite. Parasite ring and
trophozoite forms were clearly detected in the blood films throughout the study
period while the schizont form was visibly observed on day 3 post-inoculation.
Western blotting [primary antibody: monoclonal anti-MAP kinase (non-phosphorylated ERK-1/2); secondary antibody: HRP-conjugated polyclonal anti-IgG] carried out on SDS-PAGE-separated cytosolic protein samples from P. berghei-infected (70% parasitemia) erythrocytes showed
that the levels of both 42 and 44 kDa MAP kinase-immunoreactive proteins increased significantly
(p<0.05) at 70% parasitemia, by up to 21.5% and 22.3% respectively as
compared to non-infected control samples. Whether the effect of P. berghei infection at 70% parasitemia on host MAP kinase signaling is related to the MAP kinase activation remains to be further investigated.
Keyword:
Malaria; MAP kinase; Plasmodium berghei; signal transduction
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*Pengarang untuk surat-menyurat;
email: hasidah@ukm.my
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