Stigmasterol blocks cartilage degradation in rabbit model of osteoarthritis.

Abstract

Stigmasterol has been shown exihbit anti-osteoarthritic properties in vitro studies. However, the in vivo effects of stigmasterol on cartilage are still unclear. This study investigated the anti-osteoarthritic properties of stigmasterol on cartilage degradation in a rabbit model of osteoarthritis (OA). Twenty rabbits underwent bilateral anterior cruciate ligament transection (ACLT) to induce OA. Five rabbits were used as normal control. Two weeks after operation, the rabbits were randomly divided into two groups. Each group of 10 rabbits received intra-articular injection with 0.3 ml of stigmasterol in left knees and vehicle in right knees, once weekly. Group 1 was killed 6 weeks after ACLT and 2 were sacrificed 9 weeks after ACLT. The knee joints were assessed by gross morphology, histology and gene expression analysis. We found that expression of genes encoding matrix metalloproteinases (MMPs) was significantly higher while tissue inhibitors of metalloproteinase (TIMP)-1 was significantly lower in the both joints of the two OA groups compared to normal contrals. Stigmasterol reduced the cartilage degradation as assessed by histological analysis and markedly suppressed MMPs expression both in group 1 and group 2. Our results suggest that stigmasterol may be considered as a possible therapeutical agent in the treatment of OA.

Sustained intra-cartilage delivery of low dose dexamethasone using a cationic carrier for treatment of post traumatic osteoarthritis

“…Therefore, cartilage pooled from the medial side was used for gene expression analyses to elucidate early changes. Consistent with the literature, after ACLT transcriptional downregulation of ACAN and upregulation of MMP1 , MMP3 , MMP13 and ADAMTS5 (Bluteau et al , 2001; Chen et al , 2012; Hotta et al , 2005; Majima et al , 2002; Wu et al , 2008) were observed. Our findings agreed with the work of Hart and colleagues (Majima et al , 2002), who report a dramatic increase in MMP13 mRNA levels 3 weeks post ACLT in all cartilage regions, which then declined rapidly by 8 weeks, suggesting that MMP13 is involved in early remodelling of matrix in response to ACLT.…”

Stigmasterol protects against Ang II-induced proliferation of the A7r5 aortic smooth muscle cell-line

“…15 In the current study, we demonstrated that Ang II induced the cell proliferation and cell cycle arrest at the S phase, and inhibited cell apoptosis in A7r5 cells, which is in line with other findings on vascular smooth muscle cells. 10,19,20 In this study, we have provided the first evidence that treatment with stigmasterol significantly inhibits the excessive proliferation and cell cycle arrest, induce apoptosis, and counteract the detrimental effects induced by angiotensin II in A7r5 cell lines. ***P < 0.001 represents significant difference when compared with the control group (without treatment with stigmasterol or Ang II).…”

<p>Validation of the Key Active Ingredients and Anti-Inflammatory and Analgesic Effects of Shenjin Huoxue Mixture Against Osteoarthritis by Integrating Network Pharmacology Approach and Thin-Layer Chromatography Analysis</p>

“…32 Stigmasterol existing in HL and RAS, was demonstrated to block cartilage degradation in the rabbit model of OA, showing potential anti-osteoarthritic properties. 33,34 Another unique key active ingredients in FK, boswellic acid, was found significant synovial concentration and therapeutic efficacy in the mouse model. 35 It could also improve physical and functional ability and reduce the pain and stiffness according to a pilot, randomized, double-blind, placebo-controlled trial.…”