Biology subjects

Santoso, A.

Publications and source records attributed to Santoso, A..

3 recordsLinked to original sources

bioRxiv2024

The effect of Citrus reticulata peel extract containing hesperidin on inhibition of SARS-CoV-2 infection based on pseudovirus entry assays

Orange (Citrus reticulata Blanco) peel contains a flavonoid glycoside hesperidin (HSD) as the primary component. HSD, upon enzymatic hydrolysis, forms hesperetin (HST) aglycone derivate. These two flavonoids have been predicted to have in-silico affinities for ACE2 and SARS-CoV-2 spike, crucial proteins in SARS-CoV-2 infection mechanisms. However, in vitro antiviral testing of orange peel extract, HSD, and HST has not been reported. This study presents for the first time a pseudovirus entry assay approach to test the anti-SARS-CoV-2 effect of HSD, HST, and orange peel extract prepared by hydrodynamic cavitation (HCV). We used a non-virulent pseudovirus model as an alternative to the original virus to target the entry point and enable research to be conducted outside the BSL-3 facility. Based on HPLC analysis, the test results showed that HCV contained HSD at about 4% w/w. Moreover, HSD 1 and 10 M, HST 10 M, and HCV 1 g/ml showed inhibition of pseudovirus entry in 293/hACE2 cells with percentages inhibition 25.92, 37.40, 27.32, and 38.97 %, respectively. Despite HCV 1 g/ml showing about 6 % lower inhibitory activity than HSD 1 M in pseudovirus entry assay, it holds potential as a supplement or source of raw material for HSD as a SARS-CoV-2 antiviral.

pharmacology and toxicology↗

bioRxiv2023

Curcumin and turmeric extract inhibited SARS-CoV-2 pseudovirus cell entry and Spike mediated cell fusion

Turmeric extract (TE) with curcumin as its main active ingredient has been studied as a potential COVID-19 therapeutic. Curcumin has been studied in silico and in vitro against a naive SARS-CoV-2 virus, yet little is known about TEs impact on SARS-CoV-2 infection. Moreover, no study reveals the potential of both curcumin and TE on the inhibition of SARS-CoV-2 cell-to-cell transmission. Here, we investigated the effects of both curcumin and TE on inhibiting SARS-CoV-2 entry and cell-to-cell transmission using pseudovirus (PSV) and syncytia models. We performed a PSV entry assay in 293T or 293 cells expressing hACE2. The cells were pretreated with curcumin or TE and then treated with PSV with or without the test samples. Next, we carried out syncytia assay by co-transfecting 293T cells with plasmids encoding spike, hACE2, and TMPRSS2 to be treated with the test samples. The results showed that in PSV entry assay on 293T/hACE/TMPRSS2 cells, both curcumin and TE inhibited PSV entry at concentrations of 1 {micro}M and 10 {micro}M for curcumin and 1 {micro}g/ml and 10 {micro}g/ml for TE. Moreover, both curcumin and TE reduced syncytia formation compared to control cells. Our study shows that TE and curcumin are potential inhibitors of SARS-CoV-2 infection at entry points, either by direct or indirect infection models. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=164 SRC="FIGDIR/small/560070v2_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@18f3faforg.highwire.dtl.DTLVardef@19e2818org.highwire.dtl.DTLVardef@5a6670org.highwire.dtl.DTLVardef@fb82d8_HPS_FORMAT_FIGEXP M_FIG C_FIG

pharmacology and toxicology↗

bioRxiv2021

Acute Effects of Cigarette on Endothelial Nitric Oxide Synthase, Vascular Cell Adhesion Molecule 1 and Aortic Intima Media Thickness

BackgroundCigarette smoking could induce endothelial dysfunction and increase of circulating markers of inflammation by activation of monocytes. This can lead to the increased of intima media thickness (IMT) of entire blood vessel and result acceleration of atherosclerosis process. However, to our knowledge, little is known about the role of cigarette smoking in this atherosclerotic inflammatory process. ObjectiveThe aim of this study is to explore the link between cigarette smoking on endothelial nitric oxide synthase (e-NOS) and vascular cell adhesion molecule 1 (VCAM-1). MethodsAn experimental study with post-test only controlled group design was used in this study. We used 18 Wistar rats (Rattus norvegicus) randomly subdivided into 2 groups, group K (-) were given no tobacco smoking exposed, whereas group K (+) were exposed to 40 cigarettes smokes daily. After 28 days, samples were analyzed for e-NOS, VCAM-1 and aortic IMT. ResultsOur results indicate that tobacco smoke can enhance the expression of VCAM-1 on mouse cardiac vascular endothelial cell, resulting in decreased expression of e-NOS level and increased of aortic IMT. Linear regression model found that eNOS level negatively correlated wiith aortic IMT (r2 = 0.584, {beta} = -0.764, p < 0.001), whereas VCAM-1 expression did not correlate with aortic IMT (r2 = 0.197, p = 0.065). ConclusionLow e-NOS level and high VCAM-1 level observed following after cigarette smoke exposure may increase aortic IMT. Clinical significanceIncreasing evidence suggests that cigarette smoke exposure could induce VCAM-1 (enhance pro-atherogenic property),and decreased of e-NOS level (anti-atherogenic depletion). Thus, cigarette smoke may represent a significant risk factor for atherosclerosis by increasing aortic IMT. This evidence is discussed herein.

pharmacology and toxicology↗