Furthermore, we found that the level of anti-apoptotic protein Bcl-2 was decreased (approximately 2-fold) with a concomitant increase in cleaved caspase-3 (approximately 3-fold) in T2D retina compared to control.
Activation of caspase-1 activity abolished sFasL-dependent apoptosis, and suppressed Fas expression and mRNA levels of caspase-3 in neutrophils from T2DM patients.
Additionally, cellular apoptosis in rats with DM was increased, and the expression of Bcl‑2 was downregulated, while levels of Bcl‑2‑associated X and caspase‑3 were upregulated, and these observations were reversed by MLT, as determined by TUNEL and western blot analysis, respectively.
Western blot, ELISA and qRT-PCR results showed that the mRNA and protein expression profiles of Caspase-3 and Bax were highly up-regulated and that Bcl-2 was down-regulated in the T2DM-PD-p38 inhibitor group.
The colony-forming capacity of EPCs and differentiation potential of bone marrow (BM) c-Kit(+)/Sca-I(+) lineage-negative mononuclear cells (KSL) were examined in T2D mice, db/db mice and KKA<sup>y</sup> mice, using EPC colony-forming assay (EPC-CFA).
Lower TNF-α, CD11 B, fatty acid synthase, and CASP3 and higher CD11 C mRNA expression was found in SAT than in visceral adipose tissue only in the MO-T2D+group.
The hepatitis C virus (HCV) may promote pancreatic β-cell apoptosis-like cell death through a caspase 3-dependent pathway, initiating the onset of type 2 diabetes mellitus (T2DM); however, the risk factors for development of T2DM and other abnormal glycometabolic factors in HCV patients of the Chinese Han ethnicity have been poorly explored.