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Carvacrol may alleviate vascular inflammation in diabetic db/db mice
Wei Zhao1, Chunyan Deng1, Qizhen Han1
1Department of Endocrinology, The Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou 550003, P.R. China.
Abstract:
Type 2 diabetes mellitus (T2DM) is associated with chronic low‑grade inflammation. Carvacrol has been confirmed to possess anti‑inflammatory properties, but its effect on diabetic vasculature remains unknown. The aim of the present study was to investigate the possible protective effects of carvacrol against vascular endothelial inflammation. The mice were divided into four groups (n=15 per group) as follows: Non‑diabetic control mice, db/db mice, db/db mice + carvacrol (low) and db/db mice + carvacrol (high) groups. The effects of carvacrol on the pathomorphism of the thoracoabdominal aorta in db/db mice were evaluated using hematoxylin and eosin and Masson's trichrome staining. The serum levels of insulin signaling molecules, such as phosphorylated insulin receptor, phosphorylated insulin receptor substrate‑1, insulin, triglyceride (TG) and inflammatory cytokines [tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and IL‑8] were measured by ELISA. Furthermore, the protein levels of the toll‑like receptor (TLR)4/nuclear factor (NF)‑κB inflammatory signaling pathway molecules were investigated in the thoracoabdominal aorta of db/db mice and in high glucose‑induced endothelial cells. Vascular endothelial cell apoptosis and viability were assessed by using flow cytometry and Cell Counting Kit‑8 assays, respectively. The results demonstrated that carvacrol alleviated vascular endothelial cell injury. Carvacrol reduced the expression levels of insulin signaling molecules, insulin, TG and inflammatory cytokines in the serum of db/db mice. Moreover, carvacrol reduced the activation of the TLR4/NF‑κB signaling pathway in vivo and in vitro. In vitro, carvacrol inhibited high glucose‑induced endothelial cell function by promoting vascular endothelial cell apoptosis and suppressing cell viability. These findings demonstrated that carvacrol could alleviate endothelial dysfunction and vascular inflammation in T2DM.
Insights
Carvacrol, a compound with anti-inflammatory properties, was found to protect against vascular endothelial inflammation in type 2 diabetes mellitus (T2DM). It reduced inflammatory markers and improved endothelial cell function in diabetic mice.
Area of Science:
- Biochemistry
- Pharmacology
- Vascular Biology
Background:
- Type 2 diabetes mellitus (T2DM) is characterized by chronic low-grade inflammation, impacting vascular health.
- While carvacrol exhibits anti-inflammatory properties, its specific effects on diabetic vasculature were previously unknown.
- Understanding these effects is crucial for developing therapeutic strategies against T2DM-related vascular complications.
Purpose of the Study:
- To investigate the protective effects of carvacrol against vascular endothelial inflammation in a mouse model of T2DM.
- To evaluate carvacrol's impact on insulin signaling, inflammatory markers, and the toll-like receptor (TLR)4/nuclear factor (NF)-κB pathway.
- To assess carvacrol's influence on endothelial cell apoptosis and viability under high glucose conditions.
Main Methods:
- Utilized db/db mice, a model for T2DM, divided into control and carvacrol-treated groups.
- Assessed aortic pathomorphism using hematoxylin and eosin and Masson's trichrome staining.
- Measured serum insulin signaling molecules, triglycerides, inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8) via ELISA.
- Investigated TLR4/NF-κB pathway activation in aortic tissue and high glucose-induced endothelial cells.
- Evaluated endothelial cell apoptosis and viability using flow cytometry and CCK-8 assays.
Main Results:
- Carvacrol treatment alleviated vascular endothelial cell injury in db/db mice.
- Reduced serum levels of insulin signaling molecules, triglycerides, and key inflammatory cytokines.
- Inhibited the activation of the TLR4/NF-κB inflammatory signaling pathway both in vivo and in vitro.
- In vitro studies showed carvacrol suppressed high glucose-induced endothelial cell dysfunction by promoting apoptosis and reducing viability.
Conclusions:
- Carvacrol demonstrates significant protective effects against vascular endothelial inflammation in type 2 diabetes.
- It ameliorates endothelial dysfunction by modulating insulin signaling, reducing inflammation, and inhibiting the TLR4/NF-κB pathway.
- These findings suggest carvacrol as a potential therapeutic agent for managing vascular complications in T2DM.
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