Protective effect of Shenmai injection on knee articular cartilage of osteoarthritic rabbits and IL-1β-stimulated human chondrocytes
Protective effect of Shenmai injection on knee articular cartilage of osteoarthritic rabbits and IL-1β-stimulated human chondrocytes
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DOI：
10.3892/etm.2017.4349
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发表时间：
2017-06-01
影响因子：
2.7
通讯作者：
Gan, Haining
中科院分区：
文献类型：
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作者：
Yao, Nan;Chen, Neng;Gan, Haining
参麦注射液(SMI)已被广泛用于治疗多种疾病。然而，其抗骨关节炎作用尚未得到充分研究。本实验研究了参麦注射液对前交叉韧带切断兔膝关节软骨的保护作用以及对白细胞介素1β(IL-1β)刺激的人关节软骨细胞的保护作用。体内实验采用右侧后肢膝关节前交叉韧带横断术(ACLT)复制雌性新西兰大白兔膝骨性关节炎(KOA)模型。兔接受假手术或ACLT手术。在接受ACLT手术的兔中，有一半的兔在ACLT手术后，每周接受一次0.3ml参麦关节内注射，持续四周。其余兔注射等量生理盐水。随后收集软骨进行组织学评估。在体外培养的人软骨细胞中加入10 ng/mlIL-1β，加入或不加入5%和2%(v/v)的SMI，分别用Griess反应和ELISA法测定细胞培养上清液中一氧化氮(NO)和前列腺素E2(PGE2)的水平。逆转录-定量聚合酶链式反应检测软骨细胞环氧合酶-2(COX-2)、诱导型一氧化氮合酶(INOS)、基质金属蛋白酶-1、基质金属蛋白酶-13及其组织抑制物-1(TIMP-1)的mRNA表达。目前的研究结果显示，参麦注射液治疗改善了ACLT兔模型的软骨退化，并降低了NO和PGE2水平。此外，参麦注射液还能降低IL-1β刺激的人软骨细胞COX-2、iNOS、MMP1和MMP13mRNA的表达，增加TIMP-1mRNA的表达。这些结果表明，SMI抑制炎症和改善软骨降解，使其成为治疗膝关节骨性关节炎的潜在和有前途的治疗选择。
Shenmai injection (SMI) has been widely used as a therapy to treat a number of diseases. However, its antiosteoarthritic properties have not yet been fully investigated. In the present study, the protective effect of SMI on knee articular cartilage of anterior cruciate ligament transected rabbits and interleukin-1 beta (IL-1 beta)-stimulated human chondrocytes was investigated. For the in vivo study, knee osteoarthritis (KOA) was induced in female New Zealand white rabbits by anterior cruciate ligament transection (ACLT) in the knee of right hind limb. Rabbits either underwent sham surgery or ACLT surgery. Out of the rabbits receiving ACLT surgery, half of the rabbits received one 0.3 ml Shenmai intra-articular injection in the knee per week for four weeks, following ACLT surgery. The other rabbits received the same volume of normal saline solution. The cartilage was subsequently collected for histological evaluation. For the in vitro study, cultured human chondrocytes were treated with 10 ng/ml IL-1 beta in the presence or absence of 5 and 2% (v/v) SMI for 24 h. Nitric oxide (NO) and prostaglandin E2 (PGE2) levels in cell culture supernatant were assessed using a Griess reaction and ELISA respectively. The mRNA expression of cyclooxgenase-2 (COX-2), inducible nitric oxide synthase (iNOS), matrix metalloproteinase (MMP)-1, MMP-13 and tissue inhibitors of metalloproteinase-1 (TIMP-1) in chondrocytes were detected by reverse transcription-quantitative polymerase chain reaction. The results of the current study revealed that treatment with SMI ameliorated cartilage degradation in the ACLT rabbit model, and decreased levels of NO and PGE2. Furthermore, treatment with SMI decreased levels of COX-2, iNOS, MMP-1 and MMP-13 mRNA expression and increased TIMP-1 mRNA expression in IL-1 beta-stimulated human chondrocytes. These results indicate that SMI suppresses inflammation and ameliorated cartilage degradation, making it a potential and promising therapeutic option to treat KOA.