The Anti-Inflammatory and Vasodilating Effects of Three Selected Dietary Organic Sulfur Compounds from Allium Species.

Chin-Chen Chu,Heuy-Ling Chu,Pin-Der Duh,Wen-Shiann Wu,Chia-Pu Lee,Ja-Ping Shieh

doi:10.3390/jfb8010005

Abstract

The anti-inflammatory and vasodilating effects of three selected dietary organic sulfur compounds (OSC), including diallyl disulfide (DADS), dimethyl disulfide (DMDS), and propyl disulfide (PDS), from Allium species were investigated. In the anti-inflammatory activity assay, the three OSC demonstrated significant inhibition of nitric oxide (NO) and prostaglandin E2 (PGE2) production in LPS-induced RAW 264.7 cells. The expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-2) in activated RAW 264.7 cells was inhibited by the three OSC, indicating that the three OSC prevented the LPS-induced inflammatory response in RAW 264.7 cells. For the vasodilative assay, the three OSC were ineffective in producing NO in SVEC4-10 cells, but they did enhance prostacyclin (PGI2) production. The expression of COX-2 in SVEC4-10 cells was activated by DADS and DMDS. Pretreatment of SVEC4-10 cells with the three OSC decreased ROS generation in H2O2-induced SVEC4-10 cells. In addition, the three OSC significantly inhibited angiotensin-I converting enzyme (ACE). The up-regulation of PGI2 production and COX-2 expression by DADS and DMDS and the reduction of ROS generation by DADS, DMDS, and PDS in SVEC4-10 cells contributed to the vasodilative effect of the three OSC. Collectively, these findings suggest that DADS, DMDS, and PDS are potential anti-inflammatory and vasodilative mediators.

Highlights

Inflammation is typically characterized by increased permeability of the endothelial tissue and influxes of blood leukocytes into the interstitium, resulting in edema [1]
We previously reported that diallyl disulfide (DADS), dimethyl disulfide (DMDS), and propyl disulfide (PDS) play an important role in the regulation of melanin formation [12]
The nitrite levels in the culture medium were determined as an index of nitric oxide (NO) synthesis, The aubsiinligtythoe fGtrhieess trheraegeentO[S2C0]. tAos isnhflowuennicneFtighuereN2OA, pliproopdoulycstaicocnhariindeR(ALPWS)-t2re6a4te.7d mcelalscrophages was invesptirgodautecedd. hTihghe lnevietrlsitoef lneivtreitles

Summary

Introduction

Inflammation is typically characterized by increased permeability of the endothelial tissue and influxes of blood leukocytes into the interstitium, resulting in edema [1]. The activation of leukocytes (e.g., neutrophils and monocytes/macrophage) can produce immune responsive factors, such as nitric oxide (NO), cytokines, and eicosanoid mediators of the immune response [2]. The response of a cell to an increase in oxidants or inflammatory stimuli often involves the activation of numerous intracellular signaling pathways. These cytosolic pathways can regulate a host of transcriptional changes that allow the cell to respond appropriately to oxidative stress and thereby contribute to various pathological conditions [4]. NO, prostaglandin E2 (PGE2), and related enzymes have been implicated as important mediators in the inflammation process. The inhibition of iNOS and COX-2 activity and/or expression is important in all cases of inflammation

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