During the past few years, rapid advancement has been made in
understanding of the mechanisms and molecules involved in the
pathogenesis of DR. This is particularly true with regard to the role
of the angiogenesis- and vasopermeability-inducing molecule,
VEGF. It has been identified as a primary initiator of proliferative
DR, and as a potential mediator of nonproliferative retinopathy
(Aiello and Wong, 2000). It is reported that ocular VEGF levels
are elevated in diabetic rats before proliferative changes in retina
(Sone et al., 1997). Similar findings were observed in our study
where VEGF expression significantly increased in diabetic control
group. TC showed reduction in VEGF level in treated rats. This
reduction might be due to the presence of active principle, Octacosanol
in T. cordifolia, which is reported to downregulate VEGF
gene expression by inhibiting matrix metalloproteinases and
nuclear translocation of NF-jB and its DNA binding activity
(Aggarwal et al., 2011; Thippeswamy et al., 2008