Role Of Carvacrol Research Articles

Carvacrol protects mice against LPS-induced sepsis and attenuates inflammatory response in macrophages by modulating the ERK1/2 pathway

Macrophages play an important role in the development of life-threatening sepsis, which is characterized by multiorgan dysfunction, through their ability to produce inflammatory cytokines. Carvacrol is a phenolic compound that has been confirmed to possess strong anti‑inflammatory activity. In this study, we mainly investigated the effect of carvacrol on lipopolysaccharide (LPS)-induced macrophage proinflammatory responses and endotoxic shock. The results showed that carvacrol significantly reduced mouse body weight loss and ameliorated pathological damage to the liver, lung, and heart under LPS-induced sepsis. Carvacrol attenuated inflammatory responses by inhibiting the LPS-induced production of inflammatory cytokine interleukin-6 (IL-6) in vivo and in vitro. Mechanistically, carvacrol inhibited IL-6 production mainly through the ERK1/2 signalling pathway in macrophages. Furthermore, carvacrol improved the survival of septic mice. This study sheds light on the role of carvacrol in the pathogenesis of LPS-induced sepsis, and thus, its potential in treating sepsis patients may be considered.

Carvacrol Suppresses Human Osteosarcoma Cells via the Wnt/β-Catenin Signaling Pathway.

Carvacrol is a monoterpenic phenol extracted from traditional Chinese herbs, including oregano and thyme. Currently, carvacrol has been widely studied for its therapeutic role in central nervous system diseases, liver diseases and digestive system cancer. However, the role of carvacrol in osteosarcoma and its underlying molecular mechanism remain elusive. Here, we aimed to examine the anticancer effects of carvacrol on osteosarcoma. The effects of carvacrol on the osteosarcoma proliferation capacity were revealed by CCK-8 and colony formation assays. Flow cytometry and Hoechst assays were used to determine the effects of carvacrol on osteosarcoma cell apoptosis. The effect of carvacrol on migration and invasion of osteosarcoma cells was determined by wound healing and transwell tests. Protein expression was evaluated by WB assays. The suppressive effects of carvacrol on osteosarcoma in vivo were examined by a xenograft animal model, immunohistochemistry and HE staining. We demonstrated that carvacrol treatment reduced viability and inhibited the colony formation of U2OS and 143B cells in a concentration-dependent manner. Apoptotic cell number increased after exposure to carvacrol. Meanwhile, the expression of Bax increased, and that of Bcl-2 decreased by carvacrol treatment. In addition, the MMP-9 expression and migration and invasion of 143B and U2OS cells were inhibited by carvacrol. We also found that these carvacrol-induced effects on osteosarcoma are associated with the regulation of the Wnt/β-catenin signaling pathway. Our findings suggest that carvacrol suppresses proliferation, migration, invasion and promotes apoptosis in osteosarcoma cells, in part by regulating the Wnt/β-catenin signaling pathway.

Carvacrol Ameliorates Transforming Growth Factor-β1-Induced Extracellular Matrix Deposition and Reduces Epithelial-Mesenchymal Transition by Regulating The Phosphatidylinositol 3-Kinase/Protein Kinase B Pathway In Hk-2 Cells

Transforming growth factor-β1 promotes excessive extracellular matrix deposition and epithelial-mesenchymal transition of tubular epithelial cells, thus stimulating the progression of renal fibrosis. Carvacrol has been shown to alleviate cardiac and liver fibrosis and attenuate renal injury. However, the role of carvacrol on renal fibrosis has not been examined. First, measurements using Cell Counting Kit-8 showed that carvacrol reduced cell viability of tubular epithelial cell line HK-2 in a dose-dependent fashion. Second, transforming growth factor-β1 induced excessive extracellular matrix deposition in HK-2 cells with enhanced collagen I, collagen IV, and fibronectin expression. However, carvacrol decreased the expression of collagen I, collagen IV in a dose-dependent manner and fibronectin to attenuate the extracellular matrix deposition in HK-2. Third, carvacrol attenuated TGF-β1-induced decrease of E-cadherin and increase of snail, vimentin, and alpha-smooth muscle actin in HK-2 cells. Transforming growth factor-β1-induced increase in PI3K and AKT phosphorylation in HK-2 were also reversed by carvacrol. Collectively, carvacrol ameliorates renal fibrosis through inhibition of transforming growth factor-β1-induced extracellular matrix deposition and epithelial-mesenchymal transition of HK-2 cells, providing potential therapy for the treatment of renal fibrosis.

The Role of Carvacrol as Active Compound of Essential Oils in Diabetes

The Role of Carvacrol as Active Compound of Essential Oils in Diabetes

Role of carvacrol in cardioprotection against myocardial ischemia/reperfusion injury in rats through activation of MAPK/ERK and Akt/eNOS signaling pathways

Carvacrol (CAR) is a compound isolated from some essential oils, many studies have demonstrated its therapeutic potential on different diseases. This study aims to evaluate the protective effect of CAR against myocardial ischemia/reperfusion (I/R) injury in rats. Male adult rats underwent ligation of the left anterior descending coronary artery (LAD) in I/R models. Rats were treated with CAR after LAD. The levels of I/R- induced infarct size, cardiomyocyte apoptosis and cardiac functional impairment were examined. Levels of superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) were detected by western blotting. Cardiomyocytes induced by hypoxic reperfusion (H/R) injury were tested by Hoechst 33258. Our results revealed that CAR administration significantly protected the heart function, attenuated myocardial infarct size, increased SOD and CAT levels, reduced MDA level and especially decreased cardiomyocytes apoptosis. Western blotting showed that CAR treatment up-regulated phosphorylated ERK (p-ERK), while producing no impact onp38 mitogen-activated protein kinase (p38MAPK) and c-Jun N-terminal kinase (JNK). The cardioprotection of CAR was reversed by the ERK inhibitor PD-98059, demonstrating the involvement of the MAPK/ERK pathway in the anti-apoptotic mechanisms of CAR. Besides, the results in vitro also showed the protective efficiency of CAR on cardiomyocytes H/R injury. Furthermore, pretreatment with CAR markedly increased the activation of Akt/eNOS pathway in cardiomyocytes subjected to H/R, and the protective effects of CAR were abolished in the presence of the Akt inhibitor LY294002. Therefore, the cardioprotective effects of CAR may be attributed to its antioxidant and antiapoptotic activities through activations of the MAPK/ERK and Akt/eNOS signaling pathways.

In vitro pro-oxidant/antioxidant role of carvacrol, thymol and their mixture in the intestinal Caco-2 cell line

The food industry needs to provide consumers with fresh and healthy products. In this context, food packaging plays an important role. Thus, certain essential oils are being incorporated into plastic polymers to confer better preservative properties. The oregano essential oil contains carvacrol and thymol, two important polyphenols. Considering their increasing use in active food packaging, the evaluation of their suitability and safety is of great interest. In the present work, a concentration-dependent increase in the antioxidant effects of carvacrol, thymol, and their mixture (10:1) was determined using DPPH and ABTS assays. In addition, the safety of these compounds was tested in vitro. Reactive oxygen species and glutathione levels were measured after exposing cells for 24 and 48h to different concentrations of carvacrol, thymol and their mixture. The abilities of these compounds to protect against or revert the effects of H2O2 on cells were also studied. The results showed that oxidative stress plays a role in the damage induced by carvacrol and the mixture at high concentrations. However, at lower concentrations, both compounds and their mixture were shown, for the first time, to protect cells against the damage induced by the H2O2.