Hypericin suppresses osteoclast formation and wear particle-induced osteolysis via modulating ERK signalling pathway

Ouyang, Zhengxiao; Zhai, Zanjing; Li, Haowei; Liu, Xuqiang; Qu, Xinhua; Li, Xianan; Fan, Qiming; Tang, Tingting; Qin, An; Dai, Kerong

doi:10.1016/j.bcp.2014.06.009

Cited by 55 publications

(57 citation statements)

References 62 publications

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“…NF-jB has been identified as the main target for the treatment of inflammatory diseases [21,22]. To investigate the anti-inflammatory mechanism of linalool, the effects of linalool on LPS-induced NF-jB activation were detected.…”

Section: Discussionmentioning

confidence: 99%

Linalool Inhibits LPS-Induced Inflammation in BV2 Microglia Cells by Activating Nrf2

Zhou

et al. 2015

Neurochem Res

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Linalool, a natural compound of the essential oils, has been reported to have anti-inflammatory effects. This study aimed to investigate the anti-inflammatory effects and mechanism of linalool in LPS-stimulated BV2 microglia cells. BV2 microglia cells were stimulated with LPS in the presence or absence of linalool. The production of inflammatory mediators TNF-α, IL-1β, NO, and PGE2 as well as Nrf2, HO-1 expression were detected. Our results showed that linalool inhibited LPS-induced TNF-α, IL-1β, NO, and PGE2 production in a dose-dependent manner. Linalool also inhibited LPS-induced NF-κB activation. Treatment of linalool induced nuclear translocation of Nrf2 and expression of HO-1. In addition, our results showed that the anti-inflammatory effect of linalool was attenuated by transfection with Nrf2 siRNA. In conclusion, these results suggested that linalool inhibits LPS-induced inflammation in BV2 microglia cells by activating Nrf2/HO-1 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Linalool Inhibits LPS-Induced Inflammation in BV2 Microglia Cells by Activating Nrf2

Zhou

et al. 2015

Neurochem Res

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“…Hypericin has also recently been reported to have anti-inflammatory, antimicrobial, and selective anti-tumor photosensitizing effects (Kang et al ., 2001; Ritz et al ., 2007; Yow et al ., 2012). In addition, hypericin suppresses phosphorylation of several important signaling molecules, such as extracellular signal-regulated kinases (ERK), nuclear factor kappa B (NF-κB), and protein kinase C (PKC), in various cell lines (Galeotti et al ., 2010; Jain Swati et al ., 2010; Ouyang et al ., 2014). …”

Section: Introductionmentioning

confidence: 99%

Hypericin, a Naphthodianthrone Derivative, Prevents Methylglyoxal-Induced Human Endothelial Cell Dysfunction

Kim

2016

Biomol Ther (Seoul)

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Methylglyoxal (MGO) is a highly reactive metabolite of glucose which is known to cause damage and induce apoptosis in endothelial cells. Endothelial cell damage is implicated in the progression of diabetes-associated complications and atherosclerosis. Hypericin, a naphthodianthrone isolated from Hypericum perforatum L. (St. John’s Wort), is a potent and selective inhibitor of protein kinase C and is reported to reduce neuropathic pain. In this work, we investigated the protective effect of hypericin on MGO-induced apoptosis in human umbilical vein endothelial cells (HUVECs). Hypericin showed significant anti-apoptotic activity in MGO-treated HUVECs. Pretreatment with hypericin significantly inhibited MGO-induced changes in cell morphology, cell death, and production of intracellular reactive oxygen species. Hypericin prevented MGO-induced apoptosis in HUVECs by increasing Bcl-2 expression and decreasing Bax expression. MGO was found to activate mitogen-activated protein kinases (MAPKs). Pretreatment with hypericin strongly inhibited the activation of MAPKs, including P38, JNK, and ERK1/2. Interestingly, hypericin also inhibited the formation of AGEs. These findings suggest that hypericin may be an effective regulator of MGO-induced apoptosis. In conclusion, hypericin downregulated the formation of AGEs and ameliorated MGO-induced dysfunction in human endothelial cells.

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“…RANK/RANKL/OPG pathway plays an essential role in the regulation of osteoclastogenesis (Han et al., ; Zhang, Heulsmann, Tondravi, Mukherjee, & Abu‐Amer, ). RANKL binds to its receptor RANK in the osteoclast‐precursor cells and activates several key molecules to stimulate maturation of osteoclasts (Ouyang et al., ). OPG, which binds RANKL with higher affinity than RANK, acts as a decoy receptor for RANKL and inhibits osteoclasts differentiation and activation (Takahashi, Maeda, Ishihara, Uehara, & Kobayashi, ).…”

Section: Discussionmentioning

confidence: 99%

Abnormal bone remodelling activity of dental follicle cells from a cleidocranial dysplasia patient

et al. 2018

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Hypericin suppresses osteoclast formation and wear particle-induced osteolysis via modulating ERK signalling pathway

Cited by 55 publications

References 62 publications

Linalool Inhibits LPS-Induced Inflammation in BV2 Microglia Cells by Activating Nrf2

Linalool Inhibits LPS-Induced Inflammation in BV2 Microglia Cells by Activating Nrf2

Hypericin, a Naphthodianthrone Derivative, Prevents Methylglyoxal-Induced Human Endothelial Cell Dysfunction

Abnormal bone remodelling activity of dental follicle cells from a cleidocranial dysplasia patient

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