Anti-arthritic effects of chlorogenic acid in interleukin-1β-induced rabbit chondrocytes and a rabbit osteoarthritis model

Chen, Weiping; Tang, Jun; Bao, Jiapeng; Hu, Pengfei; Shi, Zhijun; Wu, Lidong

doi:10.1016/j.intimp.2010.09.021

Cited by 54 publications

(42 citation statements)

References 38 publications

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“…We investigated the in vivo effects of baicalein on cartilage in experimental OA over a period of 6 weeks, which is similar to the durations used in previous studies [26,27]. We found that the cartilage displayed OA-like changes; Therefore, 6 weeks was sufficient to induce OA using ACLT.…”

Section: Discussionmentioning

confidence: 81%

Baicalein Inhibits MMPs Expression via a MAPK-Dependent Mechanism in Chondrocytes

Chen

Xiong

et al. 2015

Cell Physiol Biochem

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Background: Baicalein is a flavonoid isolated from Scutellaria baicalensis Georgi. Here, we investigated the anti-osteoarthritic effect of baicalein in vitro and in vivo. Methods: Interleukin-1 beta (IL-1β)-induced chondrocytes were treated with different concentrations of baicalein, real-time PCR and ELISA were performed to detect the matrix metalloproteinases (MMPs) expression. Western blot was used to evaluate the mitogen-activated protein kinase (MAPK) expression. In experimental osteoarthritis (OA), rabbits were treated with baicalein, gross morphological and histological assessment was performed to evaluate the cartilage damage. Results: Baicalein significantly reduced the expression of MMPs in vitro and in vivo. Moreover, baicalein significantly reduced the phosphorylation of p38 and extracellular signal regulated kinase (ERK), but not of c-Jun N-terminal kinase (JNK). In addition, intra-articular injection of baicalein ameliorated the cartilage damage in a rabbit model of OA induced by anterior cruciate ligament transection (ACLT). Conclusions: The results indicate that baicalein may be considered as a potential agent for OA treatment.

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Section: Discussionmentioning

confidence: 81%

Baicalein Inhibits MMPs Expression via a MAPK-Dependent Mechanism in Chondrocytes

Chen

Xiong

et al. 2015

Cell Physiol Biochem

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“…CGA has been emphasized to ameliorate brain damage and edema by inhibiting MMP-2 and MMP-9 in focal cerebral ischemia . In a recent study, CGA has been shown to suppress the expression of MMP-1, MMP-3, and MMP-13 and increase TIMP-1 expression in an osteoarthritis rabbit model (Chen et al 2011). The inhibitory effect of CGA on MMPs may be a component of the mechanisms in its wound repair activity and may contribute to improved wound healing.…”

Section: Discussionmentioning

confidence: 95%

“…In this study, systemic CGA Wound repair is a well-organized series of cellular events and includes phases of inflammation, proliferation, and remodeling. Some of the processes in wound repair have implicated angiogenesis, cell migration and proliferation, formation of granulation tissue and collagen, and re-epithelialization (Brown et al 1992;Clark 1985;Stadelmann et al 1998;Shukla et al 1998). CGA resulted in more extensive capillary density (a marker of angiogenesis) and epithelialization in wound tissues.…”

Section: Discussionmentioning

confidence: 99%

“…Collagen plays a pivotal role in wound repair being a master component of connective tissue. Moreover, hydroxyproline content is commonly used as an indicator for collagen level in wound tissue (Clark 1985;Robson et al 2001;Stadelmann et al 1998). Our histopathological results had confirmed that CGA enhanced fibroblast proliferation and collagen production.…”

Section: Discussionmentioning

confidence: 99%

“…The process of skin wound repair is initiated by the local release of growth factors and cytokines in the wound area. In addition, several types of cells are recruited to the wound site, such as blood cells, endothelial cells, and fibroblasts, to assist in wound healing (Brown et al 1992;Clark 1985;Shukla et al 1998). Additionally, extracellular matrix proteins and their receptors are involved in wound repair processes, which are mediated by cytokines and growth factors (McDonald 1989).…”

Section: Introductionmentioning

confidence: 99%

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Pharmacologic overview of systemic chlorogenic acid therapy on experimental wound healing

Bağdaş

Gül

Topal

et al. 2014

Naunyn-Schmiedeberg's Arch Pharmacol

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Chlorogenic acid (CGA) is a well-known natural antioxidant in human diet. To understand the effects of CGA on wound healing by enhancing antioxidant defense in the body, the present study sought to investigate the potential role of systemic CGA therapy on wound healing and oxidative stress markers of the skin. We also aimed to understand whether chronic CGA treatment has side effects on pivotal organs or rat bone marrow during therapy. Full-thickness experimental wounds were created on the backs of rats. CGA (25, 50, 100, 200 mg/kg) or vehicle was administered intraperitoneally for 15 days. All rats were sacrificed on the 16th day. Biochemical, histopathological, and immunohistochemical examinations were performed. Possible side effects were also investigated. The results suggested that CGA accelerated wound healing in a dose-dependent manner. CGA enhanced hydroxyproline content, decreased malondialdehyde and nitric oxide levels. and elevated reduced glutathione, superoxide dismutase, and catalase levels in wound tissues. Epithelialization, angiogenesis, fibroblast proliferation, and collagen formation increased by CGA while polymorph nuclear leukocytes infiltration decreased. CGA modulated matrix metalloproteinase-9 and tissue inhibitor-2 expression in biopsies. Otherwise, high dose of CGA increased lipid peroxidation of liver and kidney without affecting the heart and muscle samples. Chronic CGA increased micronuclei formation and induced cytotoxicity in the bone marrow. In conclusion, systemic CGA has beneficial effects in improving wound repair. Antioxidant, free radical scavenger, angiogenesis, and anti-inflammatory effects of CGA may ameliorate wound healing. High dose of CGA may induce side effects. In light of these observations, CGA supplementation or dietary CGA may have benefit on wound healing.

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Intra-articular resveratrol injection prevents osteoarthritis progression in a mouse model by activating SIRT1 and thereby silencing HIF-2α

Cai

Zhang³

et al. 2015

J. Orthop. Res.

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ABSTRACT:We investigated the feasibility of the intra-articular injection of resveratrol for preventing the progression of existing cartilage degeneration in a mouse model of osteoarthritis (OA). The effects of resveratrol on the expression of silent information regulator 2 type 1 (SIRT1), hypoxia-inducible factor-2a (HIF-2a) and catabolic factors in OA cartilage was explored. OA was induced in the mouse knee via destabilization of the medial meniscus (DMM). Resveratrol was injected weekly into the operated knee beginning 4 weeks after surgery. The OA phenotype was evaluated via histological and immunohistochemical analyses at 8 weeks after DMM. Western blot analysis was performed to identify whether resveratrol modulated the interleukin (IL)-1b-induced expression of HIF-2a in human chondrocytes. Histologically, resveratrol treatment preserved the structural homeostasis of the articular cartilage and the subchondral bone. Following resveratrol injection, the expression of collagen type II was retained, but the expression of inducible nitric oxide synthase and matrix metalloproteinase-13 was reduced in OA cartilage. Moreover, the administration of resveratrol significantly induced the activation of SIRT1 and the inhibition of HIF-2a expression in mouse OA cartilage and in IL-1b-treated human chondrocytes. These findings indicate that the intra-articular injection of resveratrol significantly prevents the destruction of OA cartilage by activating SIRT1 and thereby suppressing the expression of HIF-2a and catabolic factors. Keywords: osteoarthritis; resveratrol; SIRT1; HIF-2a; catabolic factorThe chronic degenerative joint disorder, osteoarthritis (OA) remains the leading cause of long-term disability, and is characterized by abnormal articulation, joint instability, pain and loss of movement.1 Under physiological circumstances, cartilage homeostasis is maintained by an equivalent balance between anabolism and catabolism.2 However, this homeostasis is disrupted in OA, in which catabolism becomes more dominant, leading to the degradation of the cartilaginous extracellular matrix and the eventual destruction of cartilage structure.3,4 The degradation of articular cartilage involves pro-inflammatory cytokine expression, inflammation, increased matrix metalloproteinase (MMP) and aggrecanase expression, decreased extracellular matrix (ECM) synthesis, and chondrocyte apoptosis. Many factors, including biophysical and biochemical activities, have been reported to be responsible for initiating the pathogenesis of OA. Among these factors, hypoxia-inducible factor-2a (HIF-2a) was recently demonstrated to play a key role in the regulation of catabolic reactions in arthritic cartilage. 5,6 HIF-2a (also termed endothelial PAS domain protein-1, EPAS1), belong to the basic helix-loop-helix/ PAS transcription factor family.7 HIF-2a is regulated by its oxygen-dependent degradation and participates in the modulation of the hypoxic response by binding to hypoxia-responsive elements (HREs) in the promoters of target genes. 6,8 In a re...

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Anti-arthritic effects of chlorogenic acid in interleukin-1β-induced rabbit chondrocytes and a rabbit osteoarthritis model

Cited by 54 publications

References 38 publications

Baicalein Inhibits MMPs Expression via a MAPK-Dependent Mechanism in Chondrocytes

Baicalein Inhibits MMPs Expression via a MAPK-Dependent Mechanism in Chondrocytes

Pharmacologic overview of systemic chlorogenic acid therapy on experimental wound healing

Intra-articular resveratrol injection prevents osteoarthritis progression in a mouse model by activating SIRT1 and thereby silencing HIF-2α

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