Controlled Release of Interleukin-1 Receptor Antagonist from Hyaluronic Acid-Chitosan Microspheres Attenuates Interleukin-1β-Induced Inflammation and Apoptosis in Chondrocytes.
Controlled Release of Interleukin-1 Receptor Antagonist from Hyaluronic Acid-Chitosan Microspheres Attenuates Interleukin-1β-Induced Inflammation and Apoptosis in Chondrocytes.
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透明质酸-壳聚糖微球控制释放白细胞介素 1 受体拮抗剂可减轻软骨细胞中白细胞介素 1 β 诱导的炎症和细胞凋亡
DOI：
10.1155/2016/6290957
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发表时间：
2016
影响因子：
--
通讯作者：
Zhou PH
中科院分区：
文献类型：
--
作者：
Qiu B;Gong M;He QT;Zhou PH
This paper investigates the protective effect of interleukin-1 receptor antagonist (IL-1Ra) released from hyaluronic acid chitosan (HA-CS) microspheres in a controlled manner on IL-1β-induced inflammation and apoptosis in chondrocytes. The IL-1Ra release kinetics was characterized by an initial burst release, which was reduced to a linear release over eight days. Chondrocytes were stimulated with 10 ng/ml IL-1β and subsequently incubated with HA-CS-IL-1Ra microspheres. The cell viability was decreased by IL-1β, which was attenuated by HA-CS-IL-1Ra microspheres as indicated by an MTT assay. ELISA showed that HA-CS-IL-1Ra microspheres inhibited IL-1β-induced inflammation by attenuating increases in NO2 − and prostaglandin E2 levels as well as increase in glycosaminoglycan release. A terminal deoxyribonucleotide transferase deoxyuridine triphosphate nick-end labeling assay revealed that the IL-1β-induced chondrocyte apoptosis was decreased by HA-CS-IL-1Ra microspheres. Moreover, HA-CS-IL-1Ra microspheres blocked IL-1β-induced chondrocyte apoptosis by increasing B-cell lymphoma 2 (Bcl-2) and decreasing Bcl-2-associated X protein and caspase-3 expressions at mRNA and protein levels, as indicated by reverse-transcription quantitative polymerase chain reaction and western blot analysis, respectively. The results of the present study indicated that HA-CS-IL-1Ra microspheres as a controlled release system of IL-1Ra possess potential anti-inflammatory and antiapoptotic properties in rat chondrocytes due to their ability to regulate inflammatory factors and apoptosis associated genes.
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影响因子：
3.7
作者：
Oprenyeszk F;Sanchez C;Dubuc JE;Maquet V;Henrist C;Compère P;Henrotin Y
通讯作者：
Henrotin Y
影响因子：
2.3
作者：
Ma BL;Zhou PH;Xie T;Shi L;Qiu B;Wang Q
通讯作者：
Wang Q
影响因子：
2.3
作者：
Campo, Giuseppe M.;Micali, Antonio;Campo, Salvatore
通讯作者：
Campo, Salvatore
影响因子：
5.8
作者：
Al-Qadi, Sonia;Alatorre-Meda, Manuel;Remunan-Lopez, Carmen
通讯作者：
Remunan-Lopez, Carmen
影响因子：
--
作者：
Li, Xin;Ellman, Michael;Muddasani, Prasuna;Wang, James H. -C.;Cs-Szabo, Gabriella;van Wijnen, Andre J.;Im, Hee-Jeong
通讯作者：
Im, Hee-Jeong