Component Of Cinnamon Research Articles

Cinnamic Acid Attenuates Peripheral and Hypothalamic Inflammation in High-Fat Diet-Induced Obese Mice.

Obesity is closely linked to chronic inflammation in peripheral organs and the hypothalamus. Chronic consumption of a high-fat diet (HFD) induces the differentiation of Ly6chigh monocytes into macrophages in adipose tissue, the liver, and the brain, as well as the secretion of pro-inflammatory cytokines. Although cinnamon improves obesity and related diseases, it is unclear which components of cinnamon can affect macrophages and inflammatory cytokines. We performed in silico analyses using ADME, drug-likeness, and molecular docking simulations to predict the active compounds of cinnamon. Among the 82 active compounds of cinnamon, cinnamic acid (CA) showed the highest score of ADME, blood–brain barrier permeability, drug-likeness, and cytokine binding. We then investigated whether CA modulates obesity-induced metabolic profiles and macrophage-related inflammatory responses in HFD-fed mice. While HFD feeding induced obesity, CA ameliorated obesity and related symptoms, such as epididymal fat gain, insulin resistance, glucose intolerance, and dyslipidemia, without hepatic and renal toxicity. CA also improved HFD-induced tumor necrosis factor-α, fat deposition, and macrophage infiltration in the liver and adipose tissue. CA decreased Ly6chigh monocytes, adipose tissue M1 macrophages, and hypothalamic microglial activation. These results suggest that CA attenuates the peripheral and hypothalamic inflammatory monocytes/macrophage system and treats obesity-related metabolic disorders.

Effects of cinnamaldehyde on glucose-6-phosphate dehydrogenase activity, some biochemical and hematological parameters in diabetic rats

Context Diabetes is a metabolic disorder related to blood insulin deficiency and high glucose level. Cinnamaldehyde is an important component of cinnamon and has an effect on blood glucose. Objective It was aimed to investigate the the effect of cinnamaldehyde on the liver glutathione (GSH), glucose-6-phosphate dehidrogenase (G6PD) activity, blood glucose, protein, lipid and erythrocyte parameters, live weight in diabetic rats. Material and Methods Rat used for this research were divided 4 group as control, diabetic, cinnamaldehyde and diabetic + cinnamaldehyde group. The live weight and fasting blood glucose level, taken from tail vein were recorded every ten days. End of the trail the blood samples were taken from rats. Biochemical parameters with autoanalyzer and hematological parameters with blood cell counter were determined in blood. The activity of G6PD and GSH amounts were measured with ELISA in the liver tissues. Results Blood sugar, triglyceride, total cholesterol, VLDL, LDL, and urea levels increased in diabetic rats, and cinnemaldehyde significantly decreased these parameters. Cinnemaldehyde also showed a positive effect on body weight, blood total protein, and mean corpuscular volume in diabetes. A decrease in HbA1c and an increase in liver G6PD, GSH activity were found in treatment group, but these changes were not statistically significant. Conclusion In conclusion, the antidiabetic, hypolipidemic and antioxidant effects of cinnamaldehyde were determined. It has also been shown to improve anaemia, ürea levels and weight loss.

Cinnamaldehyde Enhances the Sensitivity of Gastric Cancer Cells to Oxaliplatin by Regulating the PI3K/AKT Pathway

Gastric cancer is the second leading cause of all cancer-related deaths. While chemotherapy is still the main treatment option for patients with advanced gastric cancer, it at times leads to drug resistance and treatment failure. Therefore, there is an urgent need for better pharmacotherapeutics. Cinnamaldehyde is a bioactive component of cinnamon that has been reported to exhibit a variety of biological functions, including antitumor activity with a variety of cancer types. However, its possible effect on gastric cancer remains to be explored. Herein, we have successfully constructed oxaliplatin-resistant gastric cancer cells and shown that cinnamaldehyde could enhance the inhibitory effects of oxaliplatin on cell viability, and stimulate apoptosis in gastric cancer cells. We further found that cinnamaldehyde could regulate PI3K/AKT pathway, and further enhance the sensitivity of gastric cancer cells to oxaliplatin. Therefore, cinnamaldehyde could serve as a promising therapeutic agent for drug resistant gastric cancer.

Network pharmacology-based research uncovers cold resistance and thermogenesis mechanism of Cinnamomum cassia

BackgroundCinnamomum cassia (L.) J.Presl (Cinnamon) was known as a kind of hot herb, improved circulation and warmed the body. However, the active components and mechanisms of dispelling cold remain unknown. MethodsThe effects of several Chinses herbs on thermogenesis were evaluated on body temperature and activation of brown adipose tissue. After confirming the effect, the components of cinnamon were identified using HPLC-Q-TOF/MS and screened with databases. The targets of components were obtained with TCMSP, SymMap, Swiss and STITCH databases. Thermogenesis genes were predicted with DisGeNET and GeneCards databases. The protein-protein interaction network was constructed with Cytoscape 3.7.1 software. GO enrichment analysis was accomplished with STRING databases. KEGG pathway analysis was established with Omicshare tools. The top 20 targets for four compounds were obtained according to the number of edges of PPI network. In addition, the network results were verified with experimental research for the effects of extracts and major compounds. ResultsCinnamon extract significantly upregulated the body temperature during cold exposure.121 components were identified in HPLC-Q-TOF/MS. Among them, 60 compounds were included in the databases. 116 targets were obtained for the compounds, and 41 genes were related to thermogenesis. The network results revealed that 27 active ingredients and 39 target genes. Through the KEGG analysis, the top 3 pathways were PPAR signaling pathway, AMPK signaling pathway, thermogenesis pathway. The thermogenic protein PPARγ, UCP1 and PGC1-α was included in the critical targets of four major compounds. The three major compounds increased the lipid consumption and activated the brown adipocyte. They also upregulated the expression of UCP1, PGC1-α and pHSL, especially 2-methoxycinnamaldehyde was confirmed the effect for the first time. Furthermore, cinnamaldehyde and cinnamon extract activated the expression of TRPA1 on DRG cells. ConclusionThe mechanisms of cinnamon on cold resistance were investigated with network pharmacology and experiment validation. This work provided research direction to support the traditional applications of thermogenesis.

Mechanisms of Herb-Drug Interactions Involving Cinnamon and CYP2A6: Focus on Time-Dependent Inhibition by Cinnamaldehyde and 2-Methoxycinnamaldehyde.

Information is scarce regarding pharmacokinetic-based herb-drug interactions (HDI) with trans-cinnamaldehyde (CA) and 2-methoxycinnamaldehyde (MCA), components of cinnamon. Given the presence of cinnamon in food and herbal treatments for various diseases, HDIs involving the CYP2A6 substrates nicotine and letrozole with MCA (KS = 1.58 µM; Hill slope = 1.16) and CA were investigated. The time-dependent inhibition (TDI) by MCA and CA of CYP2A6-mediated nicotine metabolism is a complex process involving multiple mechanisms. Molecular dynamic simulations showed that CYP2A6's active site accommodates two dynamic ligands. The preferred binding orientations for MCA and CA were consistent with the observed metabolism: epoxidation, O-demethylation, and aromatic hydroxylation of MCA and cinnamic acid formation from CA. The percent remaining activity plots for TDI by MCA and CA were curved, and they were analyzed with a numerical method using models of varying complexity. The best-fit models support multiple inactivator binding, inhibitor depletion, and partial inactivation. Deconvoluted mass spectra indicated that MCA and CA modified CYP2A6 apoprotein with mass additions of 156.79 (142.54-171.04) and 132.67 (123.37-141.98), respectively, and it was unaffected by glutathione. Heme degradation was observed in the presence of MCA (48.5% ± 13.4% loss; detected by liquid chromatography-tandem mass spectrometry). In the absence of clinical data, HDI predictions were made for nicotine and letrozole using inhibition parameters from the best-fit TDI models and parameters scaled from rats. Predicted area under the concentration-time curve fold changes were 4.29 (CA-nicotine), 4.92 (CA-letrozole), 4.35 (MCA-nicotine), and 5.00 (MCA-letrozole). These findings suggest that extensive exposure to cinnamon (corresponding to ≈ 275 mg CA) would lead to noteworthy interactions. SIGNIFICANCE STATEMENT: Human exposure to cinnamon is common because of its presence in food and cinnamon-based herbal treatments. Little is known about the risk for cinnamaldehyde and methoxycinnamaldehyde, two components of cinnamon, to interact with drugs that are eliminated by CYP2A6-mediated metabolism. The interactions with CYP2A6 are complex, involving multiple-ligand binding, time-dependent inhibition of nicotine metabolism, heme degradation, and apoprotein modification. An herb-drug interaction prediction suggests that extensive exposure to cinnamon would lead to noteworthy interactions with nicotine.