Effect of crotonaldehyde on the induction of COX-2 expression in human endothelial cells

2018

IJMS

Kaempferia parviflora, referred to as black ginger, has traditionally been used as a health-promoting alternative medicine. In this study, we examined the anti-inflammatory, sebostatic, and anti-Propionibacterium acnes activities of K. parviflora extract. The extract significantly down-regulated the expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), and pro-inflammatory cytokine tumor necrosis factor alpha (TNF-α) level. Moreover, the phosphorylation of IĸBα and nuclear factor-kappa B (NF-κB), and the enhanced nuclear translocation of NF-κB p65 in lipopolysaccharide-stimulated murine macrophage-like cell line (RAW 264.7) cells were markedly decreased by the extract. Notably, the main component of K. parviflora, 5,7-dimethoxyflavone, also modulated the expression of iNOS and NF-κB signal molecules in P. acnes-stimulated human keratinocyte (HaCaT) cells. Additionally, K. parviflora extract inhibited the lipogenesis of sebocytes, as evidenced by a reduced level of triglyceride and lipid accumulation in the sebocytes. The sebostatic effect was also confirmed by a reduced expression of peroxisome proliferation-activating receptors (PPAR-γ) and oil-red O staining in sebocytes. Taken together, this study suggests for the first time that K. parviflora extract could be developed as a potential natural anti-acne agent with anti-inflammatory, sebostatic, and anti-P. acnes activity.

Section: Methodsmentioning

confidence: 99%

Kaempferia parviflora Extract as a Potential Anti-Acne Agent with Anti-Inflammatory, Sebostatic and Anti-Propionibacterium acnes Activity

Jin

2018

IJMS

“…The expression of COX-2 enzyme is known to rapidly increase during inflammatory reactions, and many studies have reported that toxic components present in tobacco induce this enzyme. 20 Increased COX-2 expression promotes and exacerbates atherosclerotic inflammation. Therefore, chronic inflammation with increased COX-2 might play an important role in vascular diseases such as atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

“…Total RNA was isolated from cells using TRIzol, according to the manufacturer's instructions. Real-time reverse-transcriptase PCR was performed as previously described, 20 cDNA was synthesized using random primers and Moloney murine leukaemia virus reverse transcriptase (Invitrogen, Carlsbad, CA, USA) according to the manufacturer's instructions. Real-time reverse-transcriptase PCR analysis was performed using an StepOnePlus Real-Time PCR Instrument (Applied Biosystems, Foster City, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

Curcumin Attenuates Acrolein-induced COX-2 Expression and Prostaglandin Production in Human Umbilical Vein Endothelial Cells

Park

Jeon

et al. 2020

J Lipid Atheroscler

Self Cite

Objective Inflammation is crucial to limiting vascular disease. Previously we reported that acrolein, a known toxin in tobacco smoke, might play an important role in the progression of atherosclerosis via an inflammatory response involving cyclooxygenase-2 (COX-2) and prostaglandin production in human umbilical vein endothelial cells (HUVECs). Curcumin has been known to improve vascular function and have anti-inflammatory properties. In this study, we investigated whether curcumin prevents the induction of inflammatory response caused by acrolein. Methods Anti-inflammatory effects of curcumin were examined in acrolein-stimulated HUVECs. Induction of proteins, mRNA, prostaglandin and reactive oxygen species (ROS) were measured using immunoblot analysis, real-time reverse-transcription polymerase chain reaction, enzyme-linked immunosorbent assay and flow cytometry, respectively. Results Curcumin attenuates inflammatory response via inhibition of COX-2 expression and prostaglandin production in acrolein-induced human endothelial cells. This inhibition by curcumin results in the abolition of phosphorylation of protein kinase C, p38 mitogen-activated protein kinase, and cAMP response element-binding protein. Furthermore, curcumin suppresses the production of ROS and endoplasmic reticulum stress via phosphorylation of eukaryotic initiation factor-2α caused by acrolein. Conclusion These results suggest that curcumin might be a useful agent against endothelial dysfunction caused by acrolein-induced inflammatory response.

“…Crotonaldehyde is considered to be an extremely reactive compound and its reactivity corresponds with the mutagenic and cytotoxic effects, which manifest themselves without its prior metabolic activation [10]. Crotonaldehyde induces numerous adverse cellular effects, including inflammatory response and cell death via several mechanisms [11,12,13,14,15].…”

Section: Introductionmentioning

confidence: 99%

Autophagy in Crotonaldehyde-Induced Endothelial Toxicity

Park

et al. 2019

Molecules

Self Cite

Crotonaldehyde is an extremely toxic α,β-unsaturated aldehyde found in cigarette smoke, and it causes inflammation and vascular dysfunction. Autophagy has been reported to play a key role in the pathogenesis of vascular diseases. However, the precise mechanism underlying the role of acute exposure crotonaldehyde in vascular disease development remains unclear. In the present study, we aimed to investigate the effect of crotonaldehyde-induced autophagy in endothelial cells. Acute exposure to crotonaldehyde decreased cell viability and induced autophagy followed by cell death. In addition, inhibiting the autophagic flux markedly promoted the viability of endothelial cells exposed to high concentrations of crotonaldehyde. Crotonaldehyde activated the AMP-activated protein kinase (AMPK) and p38 mitogen-activated protein kinase (MAPK) pathways, and pretreatment with inhibitors specific to these kinases showed autophagy inhibition and partial improvement in cell viability. These data show that acute exposure to high concentrations of crotonaldehyde induces autophagy-mediated cell death. These results might be helpful to elucidate the mechanisms underlying crotonaldehyde toxicity in the vascular system and contribute to environmental risk assessment.