Freshwater Clam Extract Inhibits Inflammatory Responses in LPS-Activated Macrophages by Reducing the Activation of Mitogen-Activated Protein Kinases and NF-κB

Abstract

Recent studies demonstrated that freshwater clam (Corbicula fluminea) has lipid-lowering and hepatoprotective activities, but its effect on immune responses has not yet been addressed. Here we showed that ethanol extracts of C. fluminea (ECF) reduced nitrite oxide, interleukin-1β, interleukin-6, and tumor necrosis factor-α in lipopolysaccharide-activated macrophages. Further, ECF was fractionated into n-hexane, ethyl acetate, ethanol, and water soluble fractions. Of these, the ethyl acetate soluble fraction (EACF) had the highest capacity to inhibit pro-inflammatory mediators expression. The underlying mechanisms for the anti-inflammatory activity of EACF were demonstrated as down-regulation of ERK1/2, JNK1/2, and p38 phosphorylation and NF-κB activity. Using gas chromatography-mass spectrometric analysis EACF was found to be composed mainly of fatty acids and steroids. Our results provide evidence that freshwater clam has anti-inflammatory activity, and support the possibility for the development of freshwater clam as a health supplement or adjuvant therapeutic agent for either preventing or treating inflammation related diseases.

Freshwater clam extract supplementation improves wound healing by decreasing the tumor necrosis factor α level in blood

“…Wound healing is a biological process that occurs in at least three overlapping stages: inflammation, proliferation, and tissue remodeling . Inflammatory responses for a short and controlled duration can be beneficial because they help protect against infection; however, prolonged and acute inflammation characterized by the excessive production of inflammatory mediators can be harmful . Wound healing is not always a linear process; it can progress forward and backward through phases, depending on various intrinsic and extrinsic factors.…”

“…those from fish oil, sea cucumbers, and freshwater clams) as treatment options for a wide variety of disorders, including acute and chronic inflammation . Freshwater clam extract (FCE) products are becoming available in health food stores because of their therapeutic effects, particularly for providing hepatic protector functions and hypocholesterolemic effects . Although the traditional diet therapy of FCE has been used on liver diseases, its real mechanisms have not been well known.…”

“…Although the traditional diet therapy of FCE has been used on liver diseases, its real mechanisms have not been well known. The chemical composition of FCE includes stigmasterol, campesterol, and oleic acid, which significantly act to inhibit the transcriptional activity of nuclear factor (NF)‐ k B in lipopolysaccharide (LPS)‐stimulated macrophages . Campesterol inhibits prostaglandin E 2 and prostaglandin I 2 release, potentially by alteration of the enzymatic activities of cyclooxygenase‐2 (COX‐2) and phospholipases A2, possibly leading to a slowdown of atheromatous disease.…”

“…Oleic acid reduces the expression of inducible nitrix oxide synthase and COX‐2, as well as the production of NO and prostaglandin E 2 , by inhibiting reactive oxygen species, p38 mitogen‐activated protein (MAP) kinases, and NF‐ k B signaling pathways . Other studies have shown that increasing dosages of FCE result in a decrease of systemic lymphocyte proliferation and interleukin (IL)‐1 β , tumor necrosis factor (TNF)‐ α and IL‐6, as well as higher IL‐10 levels . Therefore, the mechanisms for the prevention or amelioration of inflammation‐associated disorders are produced by FCE as a result of the inhibition of the activation of p38 MAP kinases and NF‐ k B pathways …”

Essential Oil from the Heartwood of Taiwan fir Ameliorates LPS-induced Inflammatory Response by Inhibiting the Activation of Mitogen-activated Protein Kinase

“…Given the importance of NLRP3 inflammasome in the pathogenesis of diseases, the anti-inflammatory properties of EOTC that target NLRP3 inflammasome or specific pro-inflammatory mediator pathways might be used to improve the control of inflammationrelated disorders. Mitogen-activated protein kinase (MAPK), including ERK1/2, JNK1/2, and p38, is activated by LPS and plays important roles in the expression of inflammatory mediators in macrophages [2,3,12,16]. In the present study, we investigated whether EOTC is able to affect the activation of ERK1/2, JNK1/2, and p38 in LPSstimulated RAW 264.7 macrophages.…”