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.
Additionally, the importance of IL-1β in modulating the inflammatory response after corneal injury in patients with diabetes and controls was further elucidated.
On the other hand, although diabetes inhibits formalin-induced nociception higher protein levels of pro-inflammatory cytokine IL1-β and chemokine CINC-1/CXCL-1 were observed.
The results of immunohistochemical staining showed that the expressions of Fox01 and IL-1β in the inner plexiform layer and inner nuclear layer increased markedly in the DM group and lncRNA MEG3 transfection group when compared with those in the control group (p<0.05).
The suppression of inflammation by testosterone were observed in patients with coronary artery disease, prostate cancer and diabetes mellitus through the increase in anti-inflammatory cytokines (IL-10) and the decrease in pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α).
No differences of IL-17A, IL-1β, and TNF-α in tears were found between the diabetes with DE and normal group, suggesting different pathogenesis of diabetes DE vs nondiabetes DE.
In the subset analysis of the data from this trial, IL-1β inhibition with canakinumab was found to have beneficial effects in other cardiometabolic diseases characterized by inflammation, like diabetes, stroke, and chronic kidney disease, and also in patients with lung cancer.
When STZ was injected to induce diabetes in mice, neither hyperglycemia nor hypoinsulinemia was developed in agomelatine pretreated mice and 6 weeks after development of diabetes, agomelatine treatment significantly decreased levels of IL-1β mRNA in raphe nucleus and nucleus accumbens.
The evidence has shown that the NLRP3 inflammasome, IL-1β, thioredoxin-interacting protein (TXNIP), and pyroptosis play vital roles in the development of diabetes.
It was shown that DM resulted in severe learning and memory deficits associated with endothelial dysfunction, increased expression of TNF-α and IL-1β, increased oxidative stress levels and decreased expression of eNOS and BDNF.
Among patients with peri-implantitis, plaque index (p < 0.001), bleeding on probing (p < 0.001), probing depth (p < 0.001), marginal bone loss (p < 0.001), and whole salivary IL-1β (p < 0.001) and IL-6 (p < 0.001) levels were significantly higher in those with diabetes than in those without diabetes.
The NLRP3 inflammasome is activated by different forms of oxidative stress, and, based on the central role of IL-1β in the destruction of pancreatic islets, it could be related to the development of diabetes.
The present study implicates a strong association between cytokine TNF-α, IL-6 and IL-1β gene promoter polymorphisms and modulation of transcript levels with susceptibility to nephropathy in diabetes subjects.
Moreover, the microglia were activated and induced a large number of inflammatory cytokines TNF-α, IL-1β and IL-6 in the peri-infarct cortical tissues during cerebral I/R injury associated with DM.
It also inhibits cytokine levels, including IL-6, IL-18, IL-33, tumor necrosis factor and IL-1, and may improve insulin production and, therefore, the pathogenesis of diabetes, stroke and cardiovascular health.
There were statistical correlation between IL-1β and sIL-6R levels in gingival crevicular fluid (GCF) and HbA1c in periodontitis patients with DM (IL-1β: P=0.035, sIL-6R: P=0.040).
In general, concentric and isometric torques were lower and tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β plasma levels were higher in the groups with diabetes than in controls.
Osthole treatment decreased the co-expression levels of P2X<sub>4</sub> and glial fibrillary acidic protein (GFAP) and reduced the up-regulated expression of interleukin-1 beta (IL-1β), tumour necrosis factor-α (TNF-α), brain-derived neurotrophic factor (BDNF) and phosphorylated-p38MAPK and enhanced the down-regulation of IL-10 in DM rats.
After administration of BCA, retina concentrations of vascular endothelial growth factor, tumor necrosis factor-alpha and interleukin-1beta decreased in the 2 groups of treated rats with diabetes compared to the control group with diabetes (p<0.05).