Background: Shixiang plaster is a traditional Chinese medicine has been used to treat chronic ulcers, including diabetic ulcers. Aminoguanidine is a hydrazine derivative that inhibits the formation of advanced glycosylation end products (AGEs). This study aimed to investigate the effects of shixiang plaster and aminoguanidine on wound healing in the streptozotocin-induced rat model of diabetes and the molecular mechanisms involved. Material/Methods: Sprague-Dawley rats treated with intraperitoneal streptozotocin and given surgical wounds were divided into the untreated chronic ulcer group (n=10), the aminoguanidine group (n=10), the shixiang plaster group (n=10), and the control group with sham surgery (n=10). Granulation tissue samples underwent light microscopy to evaluate angiogenesis and immunohistochemistry to identify AGE, vascular endothelial growth factor (VEGF), and CD34 expression. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot measured mRNA and protein expression of receptor for advanced glycation end products (RAGE), vascular cell adhesion molecule-1 (VCAM-1), nuclear factor kappa B (NF-kB) and endothelial nitric oxide synthase (eNOS). Results: The shixiang plaster group showed a significant increase in angiogenesis in ulcer granulation tissue, significantly reduced expression of AGEs and increased expression of VEGF and CD34 expression in granulation tissue compared with the untreated chronic ulcer group (p<0.05). The shixiang plaster group showed significantly down-regulated expression of RAGE and VCAM-1 compared with the untreated chronic ulcer group (p<0.05). Shixiang plaster promoted angiogenesis by activating the NF-kB p65 associated pathway and eNOS activation. Conclusions: Shixiang plaster promoted healing in a rat model of diabetic ulcer through the RAGE/NF-kB and VEGF/VCAM-1/eNOS signaling pathways.
Aims: The aim of this study was to examine the effects of
sericin on diabetic cognitive impairment (DCI) in rats based on
neuroinflammation. Methods: SD rats were firstly fed with high
sugar and high fat diet for 4 weeks, and then injected with 50 mg/kg
streptozotocin intraperitoneally to establish a diabetic model. The
diabetic rats were randomly divided into 3 groups and treated with
distilled water (n=10), 500 mg/kg (n =10) and 1000 mg/kg (n=20) sericin,
respectively, by gavage once a day for 8 weeks. Before the end of the
trail, 10 rats in the 1000 mg/kg sericin group were injected with 10 μg
EX527 (a SIRT1 inhibitor) into the lateral ventricles once every other
day for 5 times. Results: Treated with sericin significantly
reduced the fasting blood glucose, improved DCI in rats. Sericin
significantly inhibited of neuroinflammation, reduced the expression of
NLRP3, TXNIP proteins and reduced cell apoptosis, while increased the
expression of SIRT1 protein in the hippocampus of diabetic rats. After
inhibiting SIRT1 with EX527, the above effect of sericin on DCI rats was
weakened. Conclusions: These results indicated that sericin may
block DCI progression in rats by inhibiting TXNIP/NLRP3
neuroinflammation and neuronal apoptosis though SIRT1.
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