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Published on: September 15, 2017
Anti-inflammatory activity of benidipine hydrochloride in LPS-activated mammalian macrophages
Hülya Servi1, Tanya Beril Korkmaz1, Furkan Ayaz2
1Faculty of Science, Department of Biotechnology, Mersin University, Mersin, Turkey.
Insights
Benidipine hydrochloride (BH), a calcium channel blocker, demonstrates anti-inflammatory effects by reducing pro-inflammatory cytokine production in macrophages. This suggests BH may help manage inflammation associated with hypertension.
Area of Science:
- Immunology
- Pharmacology
Background:
- Benidipine hydrochloride (BH) is a widely used calcium channel blocker for hypertension.
- The anti-inflammatory effects of BH on macrophages remain largely uninvestigated.
Purpose of the Study:
- To investigate the impact of benidipine hydrochloride on the inflammatory activity of J774.2 murine macrophage cells.
- To determine if BH modulates the production of key pro-inflammatory cytokines.
Main Methods:
- J774.2 murine macrophage cells were treated with benidipine hydrochloride.
- Cells were stimulated with lipopolysaccharide (LPS) in the presence or absence of BH.
- Pro-inflammatory cytokine production (IL-12p40, TNF-α, GM-CSF, IL-6) was measured.
Main Results:
- BH alone did not induce the production of pro-inflammatory cytokines (IL-12p40, TNF-α, GM-CSF, IL-6) in macrophages.
- In the presence of LPS, BH significantly reduced the production of these pro-inflammatory cytokines.
- These findings indicate an anti-inflammatory activity of benidipine hydrochloride.
Conclusions:
- Benidipine hydrochloride exhibits anti-inflammatory properties by suppressing macrophage-mediated cytokine release.
- BH may offer additional therapeutic benefits beyond blood pressure control in hypertensive patients by mitigating associated inflammation.
Abstract:
Benidipine hydrochloride (BH), a medication frequently used by the hypertension patients, acts as a calcium channel blocker. However, its effects on the macrophages have not been investigated thus far. Our goal was investigating the effect of the benidipine hydrochloride to modulate the J774.2 murine macrophage cells inflammatory activity. Our results suggest that in the absence of a standard stimulating agent (LPS) BH did not stimulate the macrophages to produce pro-inflammatory IL-12p40, TNF-α, GM-CSF and IL-6 cytokines. However, when BH was administrated to the cells in the presence of LPS as stimulating agent, it reduced the production of these pro-inflammatory cytokines. Therefore, it had anti-inflammatory activity. At the clinical setting this study suggests that BH can be utilized as hypertension drug that can suppress the inflammation associated with it.
