Rats in the diabetes mellitus group exhibited significantly decreased systolic cardiac function along with elevated expression levels of phosphorylated (p)-PKCβ<sub>2</sub>, phos-P66<sup>shc</sup>, caspase-3, malondialdehyde, collagen type I, tumor necrosis factor-α and interleukin-1β, which were accompanied by disorder in metabolic processes.
In this study, STZ exposure induced diabetes that augmented hepatic damage, which was reflected in serum enzyme markers, the cytokine network, and caspase-3 and caspase-9 levels in Group 2.
The histopathologic investigation using caspase-3, Bax, and TUNEL staining showed that the mean rank of the diabetic group was significantly higher compared with the RSV10, RSV20, and control groups (DM > RSV10 > RSV20 > control) (P < .05).
Treatment of the diabetic rats with RE improved hyperglycemia, hyperalgesia and motor deficit, suppressed caspase-3 activation and reduced the Bax:Bcl-2 ratio, suggesting that the RE has antihyperalgesic and neuroprotective effects in this rat model of STZ-induced diabetes.
When compared with control rats, rats in the DM group showed decreased amplitude and latency of the peak times in the ERG test; further, DM group rats presented increases in blood glucose, BRB permeability, a retinal capillary area density, retinal cell apoptosis with an increased number of active caspase-3-positive cells, MDA level, mGluR5 levels, and the ratio of p-JNK/JNK, and they showed reductions in body weight and SOD activity, as well as in the number of pericytes and in the pericyte coverage (all P < 0.05).
Higher levels of phosphorylated protein kinase B (p-AKT)/protein kinase B (AKT) (<i>p</i> < 0.05) and B-cell lymphoma-2 (Bcl-2) and lower levels of the apoptosis factors Bcl2-associated x (Bax) and caspase-3 were observed in the MSC-treated group than in the DM ED group (<i>p</i> < 0.05).
Cleaved caspase-3 and cleaved poly (adenosine diphosphate-ribose) polymerase measured by western blotting showed increased apoptosis with overexpressed CIDEC in diabetes.
In addition, islet transplantation attenuated the increased levels of cTn-I and CK-MB, cleaved-caspase-3 in response to DM, and ameliorated diabetic-induced cardiac hypertrophy and interstitial fibrosis, along with improved extracellular matrix (ECM) deposition.
ASE improved biomarkers of renal filtration barrier (podocin and nephrin) in D and DH groups and prevented the increased expression of caspase-3, IL-6, TNF-α and MCP-1 in both groups.
Expression levels of caspase-3, Bax and Bcl-2 mRNA and protein were significantly higher in diabetes + SAH group than in blank control group and diabetes group.
Articular cartilage thickness and GAG content were significantly lower (p < 0.05) in the OVX-Di group, which also showed a higher number of casp-3-positive chondrocytes than the other groups.
Streptozotocin-induced diabetes after 4 weeks caused smaller size of the organs, hypercontractility, histological abnormalities, increased concentrations of malondialdehyde in the serum and tissue, overexpression of oxidative stress markers, and cleaved caspase-3 as identified by immunohistochemistry in the SVs.
Diabetes was also associated with increased postischemic apoptotic cell death manifested as increases in TUNEL positive cells, cleaved-caspase-3, and ratio of Bax/Bcl-2 protein expression.
The decrease in the inner retinal thickness (<i>P</i><0.001 <i>vs</i> CTL, <i>P</i><0.01 <i>vs</i> DM) and increases in RGCs with terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (<i>P</i><0.001 <i>vs</i> CTL, <i>P</i><0.0001 <i>vs</i> DM), glial activation, and active caspase-3 (<i>P</i><0.0001 <i>vs</i> CTL, <i>P</i><0.0001 <i>vs</i> DM) were blocked in diabetic retinas of AE extract-fed mice.
We use these measurements to measure simultaneously cAMP signaling and Caspase-3 activation in pancreatic β-cells during oxidative stress and hyperglycemia, which are essential components in the pathology of diabetes.
Cell apoptosis levels were significantly increased, and Bcl‑2 was significantly decreased in the diabetes model group in contrast with that of the sham group; however, Bax and caspase‑3 were significantly increased.
In addition, the protein expression levels of phosphatidylinositol 3‑kinase (PI3K)/Akt, glutathione peroxidase and superoxide dismutase activity, glutathione and malondialdehyde content, and inducible nitric oxide synthase (iNOS), caspase‑3 and caspase‑9 activity were detected in the rats with DM.
Furthermore, both the pro-inflammatory cytokine tumour necrosis factor α (TNF-α) and the apoptosis mediator caspase-3 were up-regulated in T2DMH samples.