Algaea-X 의작용기전

Algaea-X 의작용기전

Algaea-X 의작용기전 (Overall) 물리적스트레스 / 부상조직파괴급성염증통증부종 물리적스트레스, 부상등은영향받는부위의조직의일부를파괴시키게된다. 이에따라신체는박테리아등으로부터자체방어를위하여급성염증을일으킴으로써감염으로부터신체를방어한다. 이때부작용으로통증및부종현상이발생한다. 부상이치유된후에도, 면역세포의수가정상수준으로완전히돌아가지않고, 통증에대한민감성이올라가는등, 만성통증및만성염증으로이행되는경우가많이발생한다. 미세한수준의만성염증은거의감지되기어려워신경통이나섬유근육통 (fibromyalgia) 등원인모를만성통증을일으키게된다. 만성염증은, 조직주변에산화스트레스를증가시키고, 혈액순환을떨어뜨릴뿐만아니라조직단백질을서서히파괴함으로써, 노화를촉진시키게되며, 영향받는부위에따라퇴행성관절염등을발생시킨다. 혈액순환 만성염증 조직단백질분해 통증민감성 산화스트레스 Algaea-X 는항박테리아활성, 항히스타민활성등이우수하여급성염증에처한조직이빠른시간내에정상화시키는효과가탁월하다. 뿐만아니라, 만성염증의원인, 과정및결과를동시에제어하며, 혈류를촉진함으로써조직이정상적인기능과재생과정을수행할수있도록도와주는효과가탁월하다. 따라서원인모를만성통증, 퇴행성및류마티스관절염등을근복적으로치유하는데있어서도유래없는제품이다.

Algaea-X 의작용기전 ( 급성통증및부종 ) 물리적스트레스 / 부상 물리적스트레스, 부상등에의해조직파괴가일어나게되면감염으로부터자체방어를위하여메커니즘 ( 급성염증 ) 이작동하게된다. 조직파괴 급성염증히스타민방출면역세포증가 박테리아및주변세포파괴 통증 부종 파괴된세포나침투한박테리아등의자극으로인하여히스타민이방출되고, 면역세포를부상조직주변으로집결시키게되면각종염증반응및통증이발생하게된다. 1 히스타민의작용으로혈관벽의투과성이증가하여부종이발생하게된다. 2 염증반응에의해통증물질이다량생성된다. 3 면역세포들이강력한활성산소들을방출하여박테리아및주변세포들을파괴시킨다. Algaea-X 의핵심성분인마이톨은자체적으로항박테리아활성이우수하여 (Nagayama et al, 2002; Glombitza et al, 1985) 염증자극물질을감소시켜염증유도물질인히스타민의방출을줄여주며 (Shim et al, 2009; Li et al, 2008), 염증반응을진정시키는효과가뛰어나 (Kim et al, 2008), 1 부종의원인 ( 히스타민에의한혈관벽투과성증가 ) 을효과적으로제어함으로써빠른시간내에부종을감소시킨다. 2 COX-2 단백질의발현을효과적으로억제함으로써통증물질의생성을신속히감소시킨다. 3 면역세포들의과도한작용을조율하여부상후유증 ( 만성화등 ) 을최소화한다.

Algaea-X 의작용기전 ( 만성통증 ) 부상후유증, 노화, 반복적운동스트레스 산화스트레스 NF-kB 통증민감성 혈액순환 혈관수축인자혈액응고인자 ROS 만성통증 염증단백질 염증성 cytokines COX-2, inos 부상후유증, 피로의지속적축적, 노화과정등은염증반응의마스터키역할을하는 NF-kB를활성화시키게되어만성염증을일으키게되며통증민감서이증가된다. 1 교통사고나부상등의후유증으로인한만성통증 2 지속적인운동스트레스에의한인대주변통증 3 노화과정에서오는오십견, 요통등 만성염증은, 조직주변에산화스트레스 (ROS) 를증가시키고, 혈액순환을떨어뜨릴뿐만아니라, 면역세포를더욱집결시키고, 각종염증단백질의합성을증가시킴으로써염증상태와통증을지속적으로유지시키게된다. Algae-X 의핵심성분인마이톨은 NF-kB 의활성및그로인한반응을효과적으로조율함으로써만성염증및이로인한만성통증을근원적으로제거한 다. 1 2 3 4 염증자극물질 ( 염증성 cytokine 및산화스트레스등 ) 에의해만성염증의마스터키인 NF-kB가활성화되는것을근본적으로차단한다. (Jung et al, 2009) 통증을일으키는염증단백질들인 COX-2, inos 등의발현및활성을억제한다. (Jung et al, 2009, Hwang et al, 2006, Shin et al, 2005)) 항산화능력이우수하여만성염증에의해발생하는각종활성산소들을제거함으로써만성염증이신속히사라지도록지원한다..(Ahn et al, 2007; Senevirathne et al, 2006; Kang et al, 2003, 2005) 만성염증에의한혈액순환부진현상을극복할수있는혈관확장 (Ho ng et al, 2006) 및플라즈민활성화능력 (Fukuyama et al, 1989, 19 90; Nakayama et al, 1989) 이우수하여조직수준에서의통증발생의원인을제거한다.

Algaea-X 의작용기전 ( 관절염 ) 관절부상후유증, 노화, 과체중, 무리한운동 산화스트레스 만성염증 (NF-kB 활성화 ) 혈액순환 혈관수축인자혈액응고인자 ROS 관절조직분해속도 MMPs, hyaluronidase 염증단백질 염증성 cytokines COX-2, inos 관절퇴행화, 관절통 부상후유증, 노화, 과체중, 무리한운동등으로인하여관절조직이파괴되는속도가회복되는속도에비해커지게되면, 관절조직이점차만성염증에처하게된다. 만성염증에의해조직주변에산화스트레스가증가되고, 혈액순환이감소될뿐만아니라조직단백질의분해속도가과도하게커짐으로써, 노화를촉진시키게되며, 퇴행성관절염이발생한다. 또한, 면역반응이급격히증가하는경우에는류마티스성관절염이발생한다. Algaea-X 의핵심성분인마이톨은 NF-kB와이에따른일련의염증성반응의활성화를제어하며. 과도한면역반응을진정시키는효과가탁월하며, 혈류개선효과가우수하여관절조직의회복속도를극대화시킴으로써퇴행성및류마티스성관절염및그로인한통증을효과적으로개선시킨다. 1 염증자극물질 ( 염증성 cytokine 및산화스트레스등 ) 에의해만성염증의마스터키인 NF-kB가활성화되는것을근본적으로차단한다. (Jung et al, 2009; Ryu et al, 2009) 2 통증및조직파괴를일으키는염증단백질들인 COX-2, inos 등의발현을차단하는효과가우수하다. (Ryu et al, 2009, Shin et al, 2005) 3 관절조직을형성하는 collagen, elastin 등의단백질을분해하는효소인 MMP 의발현및활성을효과적으로억제할뿐만아니라, 관절의윤활작용에중요한 hyaluronic acid를분해하는 hyaluronidase 억제효과가뛰어나다. (Kim et al, 2006; Joe et al, 2006) Bu et al, 2006; Shibata et al, 2002) 4 조직을무차별로파괴하며염증을지속시키는작용을하는활성산소 (ROS) 를효과적으로제거함으로써조직을보호하고염증을신속히종식시킬수있도록지원한다.(Ahn et al, 2007; Senevirathne et al, 2006; Kang et al, 2003, 2005) 5 만성염증에의해발생하는혈액순환부진현상을극복할수있는혈관확장 (Hong et al, 2006) 및플라즈민활성화 (Fukuyama et al, 1989, 1990; Nakayama et al, 1989) 능력이우수하다. 이에따라통증제거및조직재생속도가더욱빨라진다. 6 과도한면역작용을진정시키는효과가탁월하여자가면역에의한관절조질파괴 ( 류마티스성관절염 ) 를막아준다. (Shim et al, 2009; Li et al, 2008; Kim et al, 2008)

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