Study of molecular mechanisms of fuyuan capsule, icariin and arasaponin R1 in treatment of osteoarthritis.
- Author:
Wenliang ZHANG
1
;
Rongheng LI
;
Shumei WANG
;
Xiaoli ZHOU
;
Yu ZHONG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Capsules; Cells, Cultured; Chondrocytes; drug effects; metabolism; DNA-Binding Proteins; metabolism; Drugs, Chinese Herbal; pharmacology; therapeutic use; Flavonoids; pharmacology; therapeutic use; Gene Expression Regulation; Male; NF-kappa B; genetics; metabolism; Osteoarthritis; drug therapy; genetics; metabolism; RNA, Messenger; genetics; Rabbits; Urokinase-Type Plasminogen Activator; genetics; metabolism
- From: China Journal of Chinese Materia Medica 2011;36(15):2113-2117
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the molecular mechanisms of Fuyuan capsule serum containing, icariin and arasaponin R1 in the treatment of osteoarthritis from the urokinase-type plasminogen activator (uPA) system.
METHODChondrocytes were isolated, cultured and identified using type II collagens immunostaining. After stimulating with TNF-alpha 10 microg x L(-1), 1 h, then the chondrocytes were treatment with glucosamine hydrochloride 25 g x L(-1), 20% Fuyuan capsule serum containing, icariin 12.5 mg x L(-1), arasaponin R1 125 mg x L(-1), icariin 12.5 mg x L(-1) + arasaponin R1 125 mg x L(-1). After 2 h, expression of uPA and nuclear factor kappa B (NF-kappaB P65) mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR), the activities of NF-kappaB(P65) combine DNA were determined by electrophoretic mobility shift assays (EMSA), 1kappaBalpha were detected by Western blotting.
RESULTFuyuan capsule, icariin and arasaponin R1 could significantly reduce NF-kappaB (P65) activities and uPA mRNA expression, and increase expression of IkappaBalpha (P < 0.01), but no significant difference between all treatment groups.
CONCLUSIONFuyuan capsule and its two main active ingredients, icariin and arasaponin R1, could protect chondrocytes from damage through reducing the NF-kappaB (P65) activities, increasing the express of IkappaBalpha and then reducing uPA of chondrocytes.