Baicalein ameliorates inflammatory-related apoptotic and catabolic phenotypes in human chondrocytes

Zhang, Xiaodong; Zhu, Yingjie; Chen, Xiantao; Zhang, Yun; Zhang, Ying; Jia, Yudong; Wang, Huichao; Liu, Youwen; Xiao, Lianbo

doi:10.1016/j.intimp.2014.05.006

Cited by 45 publications

(39 citation statements)

References 36 publications

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“…In addition, MMP-1 was inhibited by baicalein in human keratinocytes [11]. Moreover, Zhang et al reported recently that baicalein inhibited MMP-3 and MMP-13 expression in chondrocytes stimulated using a mixture of IL-1β and tumor necrosis factor-α (TNF-α) [20]. Therefore, we hypothesized that baicalein may exert beneficial effects in OA via reducing MMPs activities and expression.…”

Section: Discussionmentioning

confidence: 86%

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: 86%

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

Chen

Xiong

et al. 2015

Cell Physiol Biochem

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“…It has been widely used as a therapeutic agent for microbial infection in East Asian countries. Moreover, baicalein possesses many biochemical and pharmacological benefits, including anti-tumor, anti-fibrogenic (Oh et al 2012;Shimizu 2001), anti-inflammatory (Liu et al 2014;Zhang et al 2014), and cardiovascular protective effects. Baicalein has been increasingly used against renal (Wang et al 2012), myocardial (Kong et al 2011), pulmonary (Gao et al 2013), and hepatic (Inoue and Jackson 1999;Shimizu 2000;Sun et al 2010) fibroses as a potential antioxidant.…”

Section: Introductionmentioning

confidence: 99%

Baicalein attenuates renal fibrosis by inhibiting inflammation via down-regulating NF-κB and MAPK signal pathways

Wang

Zhou

et al. 2015

J Mol Hist

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Baicalein is a natural flavonoid that possesses notable anti-inflammatory effects. In this study, we detected whether baicalein protects against inflammatory response in unilateral ureteral obstruction mice model to ameliorate tubulointerstitial fibrosis. Baicalein treatment significantly attenuated tubulointerstitial fibrosis by markedly reducing fibronectin and collagen-I. The downregulation of alpha-smooth muscle actin and upregulation of E-cadherin indicated that the epithelial-mesenchymal transition process was suppressed. Furthermore, baicalein administration blocked the infiltration of macrophages and lymphocytes, as evidenced by the significantly reduced CD68 and CD3 positive cells. Meanwhile, the mRNA expression of the pro-inflammatory cytokines tumor necrosis factor-α, interleukin-1β, and monocyte chemotactic protein in baicalein-treated groups was markedly reduced compared with the vehicle-treated group. More importantly, unilateral ureteral obstruction induced the activation of NF-κB and mitogen-activated protein kinase signal pathways to switch on inflammatory response to aggravate kidney fibrosis, but these effects were mitigated by baicalein. These data demonstrate that baicalein could inhibit inflammatory process via inactivation of NF-κB and MAPK signal pathways to execute its anti-fibrotic actions in obstructive kidney disease.

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“…The occurrence of OA cartilage damage is always accompanied by increased apoptosis of articular chondrocytes and its inhibition attenuates the severity of OA [5][6][7]. Thus chondrocyte apoptosis has gradually become one of the potential therapeutic targets for OA [8].…”

Section: Introductionmentioning

confidence: 99%

Lactoferrin Inhibits IL-1β-Induced Chondrocyte Apoptosis Through AKT1-Induced CREB1 Activation

Xue

Tu²,

Ma³

et al. 2015

Cell Physiol Biochem

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Background/Aims: Chondrocyte apoptosis is largely responsible for cartilage degeneration in osteoarthritis (OA). Interleukin-1 beta (IL-1β) is widely used as a chondrocyte apoptosis-inducing agent, while lactoferrin (LF) is an anabolic reagent which has the potential to inhibit chondrocyte apoptosis. We assessed the effects of LF on cartilage degeneration in IL-1β-induced chondrocytes and in a rat model of OA, and explored the potential molecular mechanisms involved. Methods: Human articular chondrocytes (HACs) were treated with IL-1β alone or in combination with LF. MTT and flow cytometric assays were used to detect changes after treatment with LF. Western blotting was used to examine the relevant molecules regulating apoptosis. Results: We found that IL-1β reduced the viability of HACs, whereas 200 μg/mL of LF significantly counteracted the inhibitory effect of IL-1β. LF significantly inhibited IL-1β-induced HAC apoptosis. The protein expression of the apoptotic markers Caspase-3 and PARP was also significantly reduced in the LF treatment group when analyzed by western blotting. Furthermore, we found that LF triggered CREB1 phosphorylation in IL-1β-induced HAC apoptosis through AKT1 signaling. In addition, LF promoted the repair of articular cartilage damage in a rat OA model with elevated p-CREB levels. Conclusions: These studies suggest that LF has an anti-apoptotic effect on IL-1β-induced chondrocytes, and thus may be a promising novel therapeutic agent for OA.

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Baicalein ameliorates inflammatory-related apoptotic and catabolic phenotypes in human chondrocytes

Cited by 45 publications

References 36 publications

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

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

Baicalein attenuates renal fibrosis by inhibiting inflammation via down-regulating NF-κB and MAPK signal pathways

Lactoferrin Inhibits IL-1β-Induced Chondrocyte Apoptosis Through AKT1-Induced CREB1 Activation

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