MOK, a Pharmacopuncture Medicine, Reduces Inflammatory Response through Inhibiting the Proinflammatory Cytokine Production in LPS-stimulated Mouse Peritoneal Macrophages^※

Abstract

[Abstract]Objectives : Inthisstudy,weinvestigatedtheanti-inflammatoryandanti-oxidativeeffectsof MOK,apharmacopuncturemedicine,inlipopolysaccharide(LPS)-stimulatedmouseperitoneal macrophages. Methods : PeritonealmacrophageswereisolatedfromICRmice.Primarymacrophageswere treatedwithMOKextract(1.25,2.5,5,10,and20mg/ml)for30minandthenstimulatedwith LPS(1μg/ml)fortheindicatedtimes.CytotoxicitywasmeasuredusingMTTandLDHassays. Nitricoxide(NO)productioninculturesupernatantswasmeasuredusingtheGriessassay. ThemRNAexpressionofiNOS,COX-2,proinflammatorycytokines(TNF-α,IL-1β,andIL-6) andantioxidantenzymes(HO-1andMnSOD)wasmeasuredbyRT-PCR. Results : TreatmentwithMOKextract(2.5,5,and10mg/ml)significantlydecreasedLPS-induced NOproductioninperitonealmacrophagesthroughinhibitionofiNOSexpression.Theexpression of COX-2, TNF-α, IL-1β, and IL-6 mRNA was also decreased in LPS-stimulated macrophagesupontreatmentwithMOKextract.MOKtreatmentalsoincreasedtheexpression ofHO-1andMnSODmRNAinmacrophages. Conclusion : TheseresultsindicatethatMOKexertsanti-inflammatoryandantioxidanteffects byregulatingthetranscriptionlevelsofinflammatorymediatorsandantioxidantproteinsin activatedmacrophages.※ ThisresearchwassupportedbytheKoreanHealthTechnologyR&DProjectthroughtheKorean HealthIndustryDevelopmentInstitute(KHIDI)fundedbytheMinistryofHealth&Welfare,Republic ofKorea(grantnumber:HI16C0622).

Effects of MOK, a pharmacopuncture medicine, on the TH1/TH2 immune response and antioxidation in Con A-stimulated primary mouse splenocytes

“…The endogenous components of the antioxidant system include enzymes such as SOD, glutathione peroxidase (GSPx), and HO-1 34,35) . We previously reported that the antioxidant effects of MOK extract in LPSstimulated mouse peritoneal macrophages occurred via an increase in the expressions of MnSOD and HO-1 7) . In the present study, the treatment of splenocytes with MOK increased the mRNA expression of MnSOD and HO-1.…”

“…However, comparisons of the biological activity of MOK with that of single medicines have been rarely reported. We have previously reported the anti-inflammatory and antioxidant effects of MOK extract in activated peritoneal macrophages 7) .…”

“…MOK is one of the pharmacopuncture medicines that is used to treat the meridian of fire in nature and clinical symptoms related to heart and thyroid diseases 5,6) . MOK has been reported to exhibit anti-inflammatory and antioxidant effects in in vitro 7) . Among the constituents of MOK, Calculus Bovis from Bos taurus, Ursi Fel from Ursus arctos, and Hominis Placenta have been reported as herbs that may exert immunomodulatory effects -11) .…”

MOK, a pharmacopuncture medicine, regulates thyroid dysfunction in L-thyroxin-induced hyperthyroidism in rats through the regulation of oxidation and the TRPV1 ion channel

“…MOK is a polyherbal medicine for the immuno-pharmacopuncture therapy and it is clinically used to treat the meridian of fire in nature and symptoms related to heart disease, such as fright palpitations, fearful throbbing, sleep disorders, angina pectoris, and thyroid diseases, such as hyperthyroidism, hypothyroidism, thyroid hypertrophy, and benign thyroid nodules [ 14 ]. Recently, the anti-inflammatory and antioxidative effects of MOK have been reported [ 15 ], but little scientific evidence of MOK has been found. Therefore, we investigated the therapeutic effects of MOK pharmacopuncture in an LT4-induced hyperthyroidism rat model.…”

“…Pharmacopuncture with MOK is used for the treatment of patients with thyroid diseases such as hypothyroidism, hyperthyroidism, and heart issues. Although MOK is commonly used in Korean clinics and some studies have reported its anti-inflammatory and antioxidative effects [ 15 ], it has little scientific evidence. Therefore, in this study, we investigated the effects of the pharmacopuncture with MOK on thyroid dysfunction in L-thyroxin (LT4)-induced hyperthyroidism rats, and the possible mechanism.…”