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Published on: January 28, 2020
Opium may affect coronary artery disease by inducing inflammation but not through the expression of CD9, CD36, and
Mohammad Amin Momeni-Moghaddam1,2, Gholamreza Asadikaram3,4, Mohammad Masoumi5
1Nutrition and Biochemistry, Gonabad University of Medical Sciences, Gonabad, Iran (the Islamic Republic of).
Abstract:
The molecular mechanisms of opium with regard to coronary artery disease (CAD) have not yet been determined. The aim of the present study was to evaluate the effect of opium on the expression of scavenger receptors including CD36, CD68, and CD9 tetraspanin in monocytes and the plasma levels of tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), malondialdehyde (MDA), and nitric oxide metabolites (NOx) in patients with CAD with and without opium addiction. This case-control study was conducted in three groups: (1) opium-addicted patients with CAD (CAD+OA, n=30); (2) patients with CAD with no opium addiction (CAD, n=30); and (3) individuals without CAD and opium addiction as the control group (Ctrl, n=17). Protein and messenger RNA (mRNA) levels of CD9, CD36, and CD68 were evaluated by flow cytometry and reverse transcription-quantitative PCR methods, respectively. Consumption of atorvastatin, aspirin, and glyceryl trinitrate was found to be higher in the CAD groups compared with the control group. The plasma level of TNF-α was significantly higher in the CAD+OA group than in the CAD and Ctrl groups (p=0.001 and p=0.005, respectively). MDA levels significantly increased in the CAD and CAD+OA groups in comparison with the Ctrl group (p=0.010 and p=0.002, respectively). No significant differences were found in CD9, CD36, CD68, IFN-γ, and NOx between the three groups. The findings demonstrated that opium did not have a significant effect on the expression of CD36, CD68, and CD9 at the gene and protein levels, but it might be involved in the development of CAD by inducing inflammation through other mechanisms.
Insights
Opium addiction did not alter scavenger receptor expression (CD36, CD68, CD9) in coronary artery disease (CAD) patients. However, opium may contribute to CAD via inflammatory pathways, evidenced by increased tumor necrosis factor alpha (TNF-α) and malondialdehyde (MDA).
Area of Science:
- Cardiovascular Disease Research
- Molecular Biology
- Immunology
Background:
- Coronary Artery Disease (CAD) is a significant health concern with incompletely understood molecular underpinnings.
- The specific impact of opium on CAD pathogenesis, particularly concerning inflammatory markers and scavenger receptor expression, remains largely undetermined.
- Opium's complex chemical composition suggests potential interactions with cardiovascular disease pathways.
Purpose of the Study:
- To investigate the effect of opium addiction on the expression of scavenger receptors (CD36, CD68, CD9) in monocytes of patients with CAD.
- To assess plasma levels of key inflammatory markers, including tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), malondialdehyde (MDA), and nitric oxide metabolites (NOx), in CAD patients with and without opium addiction.
- To elucidate the molecular mechanisms linking opium use to the development or progression of coronary artery disease.
Main Methods:
- A case-control study design involving three groups: opium-addicted CAD patients (CAD+OA), non-addicted CAD patients (CAD), and a control group (Ctrl).
- Quantification of scavenger receptor (CD9, CD36, CD68) protein and mRNA expression using flow cytometry and reverse transcription-quantitative PCR.
- Measurement of plasma levels of TNF-α, IFN-γ, MDA, and NOx using appropriate biochemical assays.
Main Results:
- Plasma levels of TNF-α were significantly elevated in the CAD+OA group compared to both CAD and Ctrl groups.
- MDA levels were significantly increased in both CAD and CAD+OA groups relative to the Ctrl group.
- No significant differences were observed in the expression of CD9, CD36, CD68, or plasma levels of IFN-γ and NOx across the three study groups.
Conclusions:
- Opium addiction does not appear to significantly affect the gene or protein expression of CD36, CD68, and CD9 in monocytes of CAD patients.
- Opium may contribute to CAD pathogenesis through inflammatory mechanisms distinct from the evaluated scavenger receptors, as indicated by elevated TNF-α.
- Further research is warranted to explore alternative inflammatory pathways through which opium might influence the development of coronary artery disease.
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