Ocimum sanctum L. (OS) leaves have been shown to have a potential for lipid-lowering action. The present study was conducted to evaluate the anti-hyperlipidaemic ability of the EO extracted from OS leaves in rats fed with a high cholesterol (HC) diet. EO of OS leaves was extracted using the hydrodistillation method and its chemical composition was further determined by GC-MS. The results showed that phenylpropanoid compounds (eugenol and methyl eugenol) were the major components of the EO. There were no significant differences in body weight gain, food intake, and heart weight in all groups of rats. The HC diet apparently raised the serum total cholesterol, LDL-C and atherogenic index without significant effect on serum triglyceride, whereas it decreased the HDL-C level. The EO significantly decreased serum total cholesterol, LDL-C, triglyceride and atherogenic index whereas no significant effect on HDL-C was observed. EO depressed a high level of liver total cholesterol and triglyceride whereas no significant effect on both lipids excreted in faeces was found. It can be concluded that the EO extracted from OS leaves contributes to a lipid-lowering action in HC rats. Its antihyperlipidaemic action is predominantly due to the suppression of liver lipid synthesis. Phenylpropanoid compounds, the main composition of EO are possibly responsible for the lipid-lowering effect.

Most cases of dengue virus infection are mild, but severe cases can be fatal. Therefore, identification of factors associated with dengue severity is essential to improve patient outcomes and reduce mortality. The objective of this study was to assess associations between nutritional status and dengue severity among Thai children and adolescents. This retrospective cross-sectional study was based on the medical records of 355 patients with dengue treated at the Hospital for Tropical Disease (Bangkok, Thailand) from 2017 to 2019. Subjects were Thai children aged less than 18 years with dengue virus infection confirmed by positive NS1 antigen or IgM. The 1997 and 2009 World Health Organization (WHO) dengue classifications were used to define disease severity and body mass index for age while the WHO growth chart was used to classify nutritional status. The proportions of patients with dengue fever who were underweight, normal weight, and overweight were 8.8%, 61.5%, and 29.7%, respectively. The proportions of patients with dengue haemorrhagic fever (DHF) who were underweight, normal weight, and overweight were 10.2%, 66.1%, and 23.7%, respectively. The proportions of patients with non-severe dengue who were underweight, normal weight, and overweight were 8.6%, 60.9%, and 30.5%, respectively; the same proportions of patients with severe dengue were 10.5%, 67.1%, and 22.4%, respectively. Higher proportions of patients with severe plasma leakage (DHF grade III and IV) were overweight compared with those with mild plasma leakage (DHF grade I and II) (45.5% vs. 18.8%). No difference in nutritional status was observed in patients with different dengue severity.

Background The pathogenic mechanisms underlying the increased vascular permeability in dengue hemorrhagic fever (DHF) are not well understood. Enhanced cellular immune activation, especially activation of serotype-cross reactive T cells, has been implicated in plasma leakage in DHF. Changes in several biological markers and mediators including cytokines, chemokines, angiogenic factors and their receptors have been shown to correlate with disease severity. A decline in plasma levels of a soluble form of vascular endothelial growth factor receptor 2 (VEGFR2), a receptor of vascular endothelial growth factor (VEGF), has been associated with plasma leakage in dengue patients. Objective We aimed to investigate the effect of dengue virus (DV)-specific CD8+ T cells on the expression of VEGFR2 on endothelial cells. Method An in vitro model was developed in which dengue virus-specific CD8+ T cells generated from peripheral blood mononuclear cells (PBMCs) of DHF patients were co-cultured with antigen-presenting cells, human umbilical vein endothelial cells (HUVECs) and activated with DV non-structural protein 3 (NS3) peptides. The expression of VEGFR2 by endothelial cells was measured. Results DV-specific CD8+ T cells were serotype cross-reactive. Activation of DV-specific CD8+ T cells resulted in down-regulation of soluble VEGFR2 production and an up-regulation of cell-associated VEGFR2. Conclusions Our findings indicate that activation of DV-specific T cell is associated with modulation of VEGFR2 expression that may contribute to increased VEGF responsiveness and vascular permeability.