Peran Mangiferin Sebagai Inhibitor Enzim Kolagenase Dan Elastase

Devi Maulina

doi:10.54957/ijhs.v1i1.41

Peran Mangiferin Sebagai Inhibitor Enzim Kolagenase Dan Elastase

Indonesian Journal of Health Science ◽

10.54957/ijhs.v1i1.41 ◽

2021 ◽

Vol 1 (1) ◽

pp. 4-9

Author(s):

Devi Maulina

Keyword(s):

Reactive Oxygen Species ◽

Reactive Oxygen ◽

Oxygen Species

Reactive Oxygen Species (ROS) mampu menyebabkan penuaan dini dengan cara menghilangkan elastisitas kulit sehingga kulit menjadi keriput, kendur, dan mengalami pigmentasi. ROS dapat meningkatkan ekspresi enzim-enzim proteinase seperti matriks metaloproteinase (MMPs) dan protease serin. Enzim tersebut bertanggung jawab dalam mendegradasi kolagen dan elastin yang merupakan komponen protein dalam matriks ekstraselular (ECM) yang berperan dalam menunjang struktur dan sifat fisik kulit. Mangiferin telah terbukti aktivitasnya sebagai antioksidan dengan mengurangi kelebihan ROS didalam sel. Penelitian ini merupakan literatur review peran mangiferin menghambat kerja enzim kolagenase dan elastase yang menyebabkan kerusakan kolagen dan elastin sehingga tanda tanda penuaan dapat dicegah.

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Mitochondria as a source of reactive oxygen species

Biochemical Journal ◽

10.1042/bj20090056 ◽

2009 ◽

pp. c3 ◽

Cited By ~ 1

Author(s):

Helena M. Cochemé ◽

Michael P. Murphy

Keyword(s):

Reactive Oxygen Species ◽

Reactive Oxygen ◽

Oxygen Species

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Clinical aspects of reactive oxygen and nitrogen species

Biochemical Society Symposium ◽

10.1042/bss0710121 ◽

2004 ◽

Vol 71 ◽

pp. 121-133 ◽

Cited By ~ 25

Author(s):

Ascan Warnholtz ◽

Maria Wendt ◽

Michael August ◽

Thomas Münzel

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Risk Factor ◽

Endothelial Dysfunction ◽

Vascular Tissue ◽

Rapid Development ◽

Reactive Oxygen ◽

Clinical Aspects ◽

No Production ◽

Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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