N-(p-Coumaryol) tryptamine (CT), a phenolic amide, has been reported to exhibit anti-oxidant and anti-inflammatory activities. However, the underlying mechanism by which CT exerts its pharmacological properties has not been clearly demonstrated. The objective of this study is to elucidate the anti-inflammatory mechanism of CT in lipopolysaccharide (LPS)-challenged RAW264.7 macrophage cells. CT significantly inhibited LPS-induced extracellular secretion of pro-inflammatory mediators such as nitric oxide (NO) and PGE2, and protein expressions of iNOS and COX-2. In addition, CT significantly suppressed LPS-induced secretion of pro-inflammatory cytokines such as TNF-alpha and IL-1beta. To elucidate the underlying anti-inflammatory mechanism of CT, involvement of MAPK and Akt signaling pathways was examined. CT significantly attenuated LPS-induced activation of JNK/c-Jun, but not ERK and p38, in a concentration-dependent manner. Interestingly, CT appeared to suppress LPS-induced Akt phosphorylation. However, JNK inhibition, but not Akt inhibition, resulted in the suppression of LPS-induced responses, suggesting that JNK/c-Jun signaling pathway significantly contributes to LPS-induced inflammatory responses and that LPS-induced Akt phosphorylation might be a compensatory response to a stress condition. Taken together, the present study clearly demonstrates CT exerts anti-inflammatory activity through the suppression of JNK/c-Jun signaling pathway in LPS-challenged RAW264.7 macrophage cells.
Cytokines ; Dinoprostone ; Macrophages ; Nitric Oxide ; Phenol ; Phosphorylation ; Tumor Necrosis Factor-alpha

Derivatives of caffeic acid have been reported to possess diverse pharmacological properties such as anti-inflammatory, anti-tumor, and neuroprotective effects. However, the biological activity of methyl p-hydroxycinnamate, an ester derivative of caffeic acid, has not been clearly demonstrated. This study aimed to elucidate the anti-inflammatory mechanism of methyl p-hydroxycinnamate in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Methyl p-hydroxycinnamate significantly inhibited LPS-induced excessive production of pro-inflammatory mediators such as nitric oxide (NO) and PGE2 and the protein expression of iNOS and COX-2. Methyl p-hydroxycinnamate also suppressed LPS-induced overproduction of pro-inflammatory cytokines such as IL-1beta and TNF-alpha. In addition, methyl p-hydroxycinnamate significantly suppressed LPS-induced degradation of IkappaB, which retains NF-kappaB in the cytoplasm, consequently inhibiting the transcription of pro-inflammatory genes by NF-kappaB in the nucleus. Methyl p-hydroxycinnamate exhibited significantly increased Akt phosphorylation in a concentration-dependent manner. Furthermore, inhibition of Akt signaling pathway with wortmaninn abolished methyl p-hydroxycinnamate-induced Akt phosphorylation. Taken together, the present study clearly demonstrates that methyl p-hydroxycinnamate exhibits anti-inflammatory activity through the activation of Akt signaling pathway in LPS-stimulated RAW264.7 macrophage cells.
Cytokines ; Cytoplasm ; Dinoprostone ; Macrophages ; Neuroprotective Agents ; NF-kappa B ; Nitric Oxide ; Phosphorylation* ; Tumor Necrosis Factor-alpha

Derivatives of caffeic acid have been reported to possess diverse pharmacological properties such as anti-inflammatory, anti-tumor, and neuroprotective effects. However, the biological activity of methyl p-hydroxycinnamate, an ester derivative of caffeic acid, has not been clearly demonstrated. This study aimed to elucidate the anti-inflammatory mechanism of methyl p-hydroxycinnamate in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Methyl p-hydroxycinnamate significantly inhibited LPS-induced excessive production of pro-inflammatory mediators such as nitric oxide (NO) and PGE2 and the protein expression of iNOS and COX-2. Methyl p-hydroxycinnamate also suppressed LPS-induced overproduction of pro-inflammatory cytokines such as IL-1beta and TNF-alpha. In addition, methyl p-hydroxycinnamate significantly suppressed LPS-induced degradation of IkappaB, which retains NF-kappaB in the cytoplasm, consequently inhibiting the transcription of pro-inflammatory genes by NF-kappaB in the nucleus. Methyl p-hydroxycinnamate exhibited significantly increased Akt phosphorylation in a concentration-dependent manner. Furthermore, inhibition of Akt signaling pathway with wortmaninn abolished methyl p-hydroxycinnamate-induced Akt phosphorylation. Taken together, the present study clearly demonstrates that methyl p-hydroxycinnamate exhibits anti-inflammatory activity through the activation of Akt signaling pathway in LPS-stimulated RAW264.7 macrophage cells.
Cytokines ; Cytoplasm ; Dinoprostone ; Macrophages ; Neuroprotective Agents ; NF-kappa B ; Nitric Oxide ; Phosphorylation* ; Tumor Necrosis Factor-alpha

Hydroxycinnamic acids have been reported to possess numerous pharmacological activities such as antioxidant, anti-inflammatory, and anti-tumor properties. However, the biological activity of 1-p-coumaroyl beta-D-glucoside (CG), a glucose ester derivative of p-coumaric acid, has not been clearly examined. The objective of this study is to elucidate the anti-inflammatory action of CG in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage cells. In the present study, CG significantly suppressed LPS-induced excessive production of pro-inflammatory mediators such as nitric oxide (NO) and PGE2 and the protein expression of iNOS and COX-2. CG also inhibited LPS-induced secretion of pro-inflammatory cytokines, IL-1beta and TNF-alpha. In addition, CG significantly suppressed LPS-induced degradation of IkappaB. To elucidate the underlying mechanism by which CG exerts its anti-inflammatory action, involvement of various signaling pathways were examined. CG exhibited significantly increased Akt phosphorylation in a concentration-dependent manner, although MAPKs such as Erk, JNK, and p38 appeared not to be involved. Furthermore, inhibition of Akt/PI3K signaling pathway with wortmannin significantly, albeit not completely, abolished CG-induced Akt phosphorylation and anti-inflammatory actions. Taken together, the present study demonstrates that Akt signaling pathway might play a major role in CG-mediated anti-inflammatory activity in LPS-stimulated RAW264.7 macrophage cells.
Coumaric Acids ; Cytokines ; Dinoprostone ; Glucose ; Inflammation* ; Macrophages ; NF-kappa B ; Nitric Oxide ; Phosphorylation* ; Tumor Necrosis Factor-alpha

Objectives: The prevalence of posttraumatic stress disorder (PTSD) has increased, particularly among individuals who have recovered from coronavirus disease 2019 (COVID-19) infection. Health literacy is considered a “social vaccine” that helps people respond effectively to the pandemic. We aimed to investigate the association between long COVID-19 and PTSD, and to examine the modifying role of health literacy in this association. Methods: A cross-sectional study was conducted at 18 hospitals and health centers in Vietnamfrom December 2021 to October 2022. We recruited 4,463 individuals who had recovered from COVID-19 infection for at least 4 weeks. Participants provided information about their sociodemographics, clinical parameters, health-related behaviors, health literacy (usingthe 12-item short-form health literacy scale), long COVID-19 symptoms and PTSD (Impact Event Scale-Revised score of 33 or higher). Logistic regression models were used to examine associations and interactions. Results: Out of the study sample, 55.9% had long COVID-19 symptoms, and 49.6% had PTSD.Individuals with long COVID-19 symptoms had a higher likelihood of PTSD (odds ratio [OR], 1.86; 95% confidence interval [CI], 1.63–2.12; p < 0.001). Higher health literacy was associated with a lower likelihood of PTSD (OR, 0.98; 95% CI, 0.97–0.99; p = 0.001). Compared to those without long COVID-19 symptoms and the lowest health literacy score, those with long COVID-19 symptoms and a 1-point health literacy increment had a 3% lower likelihood of PTSD (OR, 0.97; 95% CI, 0.96–0.99; p = 0.001). Conclusion Health literacy was found to be a protective factor against PTSD and modified the negative impact of long COVID-19 symptoms on PTSD.

Background: Suicide continues to be a leading cause of death worldwide. Recently, more than 45,000 children in the age group of 10 to 19 years died by suicide, making it the second leading cause of death in the age group of 15 to 19, surpassed only by traffic accidents, tuberculosis, and fighting. Objective: To determine the prevalence of suicidal ideation among adolescents whose parents are separated/divorced; and to explore the factors associated with suicidal ideation and describe adverse experiences among adolescents. Methods: A cross-sectional descriptive study was conducted in 309 adolescents with separated/separated parents in Hue City. Data was collected through direct interviews using a structured questionnaire. Suicidal ideation was defined as the presence of thoughts or plans related to suicide within the last 12 months. Multivariate logistic regression was applied to identify factors associated with suicidal ideation in adolescents with separated/ separated parents. Results: The study found that 15.5% (95% CI:11.7 - 20.1) of adolescents with separated /separated parents reported experiencing suicidal thoughts, in which men accounted 8.4% (95% CI:5.6 – 11.2) and women accounted 7.1% (95% CI:4.5 - 10.6). Several factors were identified as increasing the risk of suicidal ideation, including alcohol use (OR = 3.24; 95% CI:1.42 - 7.42), hyperactivity/inattention (OR = 4.96; 95% CI:1.58 - 15.605), and a poor quality of family relationships (OR = 4.82; 95% CI:1.26 - 18.50). On the contrary, certain factors were found to reduce the risk, including being in the 14-15 age group of 14-15 (OR = 0.26; 95% CI:0.10 - 0.69) and participating in physical activity (OR = 0.44; 95% CI:0.21 – 0.94). Conclusions: The research highlights a significant percentage of adolescents with separated / divided parents who experience suicidal ideation. Therefore, it is imperative for families, schools, and society to develop comprehensive strategies to monitor and address various risky behaviours among students simultaneously.