Medicinus - Dexa Medica

22
research original article
Figure 4a.
Figure 4b.
Figure 4. Inhibition in the proliferation of Vascular Smooth Muscle Cells
(VSMC) in the presence and absence of serum after treatment with DLBS1033
(a) and VSMC migration in the presence of angiotensin II and DLBS1033.
Figure 5a.
Figure 5b.
Figure 5. Effect of 0.5 μg/ml DLBS1033 on expression of JAK1 (a) and STAT1 (b).
MEDICINUS 24(1), January 2011
DISCUSSION
There are increasing evidences that
platelets play an important role in the
development of atherosclerosis and antiplatelet
therapy has become a useful
means for preventing this disease. This
present study was undertaken to investigate
the role of DLBS1033, a bioactive
protein fraction, in preventing cardiovascular
disease by observing its effect on
inflammatory and plaque stabilization
systems. Inflammation plays a role in all
stages of atherothrombosis, the underlying
cause of approximately 80% of all
sudden cardiac death. 8 This study was
carried out using monocytic and vascular
smooth muscle cells (VSMC) treated with
DLBS1033; and genes which have been
known to contribute in the inflammatory
system and plaque stabilization were isolated
from the cells.
To investigate DLBS1033 effect
on inhibiting inflammation, here, we
first examined the expression of NF-kB,
a transcription factor and function as the
central player in a chronic inflammatory
disease development. 9 DLBS1033 was
seen to reduce the expression of NF-kB
(Fig. 1a). This gene has a role in signaling
pathway of atherosclerosis. In addition,
the suppression of NF-kB inhibited the
production or activation of other prima