Artesunate inhibits RANKL‐induced osteoclastogenesis and bone resorption in vitro and prevents LPS‐induced bone loss in vivo

Wei, Cheng Ming; Liu, Qian; Song, Fang; Lin, Xi; Su, Yeping; Xu, Jiake; Huang, Lin; Zong, Shao Hui; Zhao, Jinmin

doi:10.1002/jcp.25907

Cited by 41 publications

(42 citation statements)

References 38 publications

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“…Song et al showed that eriodictyol was potentially useful for the prevention of osteoporosis through inhibiting osteoclast formation and function . Achyranthes bidentata polysaccharide, berberine sulphate, nitidine chloride, artesunate and so on were also found to be potential therapeutic candidates for the prevention or treatment of osteoporosis . Other studies also investigated the osteoporotic effects of compounds such as magnolol and polysaccharides …”

Section: Discussionmentioning

confidence: 99%

Asperpyrone A attenuates RANKL‐induced osteoclast formation through inhibiting NFATc1, Ca²⁺ signalling and oxidative stress

Chen

Wang

Qiu

et al. 2019

J Cellular Molecular Medi

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Imbalance of osteoblast and osteoclast in adult leads to a variety of bone‐related diseases, including osteoporosis. Thus, suppressing the activity of osteoclastic bone resorption becomes the main therapeutic strategy for osteoporosis. Asperpyrone A is a natural compound isolated from Aspergillus niger with various biological activities of antitumour, antimicrobial and antioxidant. The present study was designed to investigate the effects of Asperpyrone A on osteoclastogenesis and to explore its underlining mechanism. We found that Asperpyrone A inhibited RANKL‐induced osteoclastogenesis in a dose‐dependent manner when the concentration reached 1 µm, and with no cytotoxicity until the concentration reached to 10 µm. In addition, Asperpyrone A down‐regulated the mRNA and protein expression of NFATc1, c‐fos and V‐ATPase‐d2, as well as the mRNA expression of TRAcP and Ctsk. Furthermore, Asperpyrone A strongly attenuated the RNAKL‐induced intracellular Ca2+ oscillations and ROS (reactive oxygen species) production in the process of osteoclastogenesis and suppressed the activation of MAPK and NF‐κB signalling pathways. Collectively, Asperpyrone A attenuates RANKL‐induced osteoclast formation via suppressing NFATc1, Ca2+ signalling and oxidative stress, as well as MAPK and NF‐κB signalling pathways, indicating that this compound may become a potential candidate drug for the prevention or treatment of osteoporosis.

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Section: Discussionmentioning

confidence: 99%

Asperpyrone A attenuates RANKL‐induced osteoclast formation through inhibiting NFATc1, Ca²⁺ signalling and oxidative stress

Chen

Wang

Qiu

et al. 2019

J Cellular Molecular Medi

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“…Mice bone marrow–derived macrophages (BMMs) were collected and cultured as described by Wei . Briefly, C57 BL/6 male mice were killed by cervical dislocation.…”

Section: Methodsmentioning

confidence: 99%

“…We induced OC differentiation as previously described . BMMs were cultivated in α‐MEM supplemented with 30 ng/mL of M‐CSF, 10% FBS, and 100 ng/mL of RANKL.…”

Section: Methodsmentioning

confidence: 99%

Ligustilide suppresses RANKL‐induced osteoclastogenesis and bone resorption via inhibition of RANK expression

Wang

Feng

et al. 2019

J of Cellular Biochemistry

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Osteoclast (OC) is the only cell involved in bone resorption. Dysfunction of OCs leads to a variety of bone diseases. Ligustilide (LIG) is the main component of the volatile oil isolated and purified from Angelica sinensis. LIG exerts many pharmacological activities, but its effects on osteoclastogenesis and bone resorption are still unclear. Our study showed that LIG inhibited receptor activator of nuclear factor‐κB (NF‐κB) ligand‐induced OC formation and activation in a dose‐dependent manner. Additionally, LIG downregulated the messenger RNA (mRNA) expression of OC‐specific genes, such as V‐ATPase d2, tartrate‐resistant acid phosphatase, a dendritic cell‐specific transmembrane protein, cathepsin K, and nuclear factor of activated T cells cl. Furthermore, LIG blocked the activation of NF‐κB/extracellular signal‐regulated kinase/p38/immunoreceptor tyrosine‐based activation motif signaling pathways. Crucially, the expression of tumor necrosis factor receptor‐associated factor 6 proteins and the expression of receptor activator of NF‐κB mRNA were inhibited by LIG. However, LIG did not affect the formation and mineralization of osteoblasts. Collectively, this observation suggests that LIG may serve as a promising agent for the prevention and treatment of diseases caused by abnormal bone resorption.

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“…The previous studies have been proven that many plants, such as artesunate [37] and picrasidine I [38] are helpful for lytic bone disease treatment. Mon is a alkaloid derived from the seeds of the crotalaria spectabilis plant, has a therapeutic effect on cancers，such as skin cancer and cervical cancer [15].…”

Section: Discussionmentioning

confidence: 99%

“…Unfortunately, high dose (60 mg/kg) of Mon can induce hypertension in animals via receiving an intraperitoneal injection after 21 days [17]. However, Mon was merely injected over the local calvarium with 2 mg/kg or 5mg/kg every two days for 7 days in this study, according to previous report [37]. Importantly, to detect the potential side effects of Mon in our study, the pathological examination of liver, kidney and spleen have been done, and the results showed that Mon had no effect on them (Fig.…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 99%

Monocrotaline Suppresses RANKL-Induced Osteoclastogenesis In Vitro and Prevents LPS-Induced Bone Loss In Vivo

Wei

Xiong

et al. 2018

Cell Physiol Biochem

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Background/Aims: Extensive osteoclast formation plays a critical role in bone diseases, including rheumatoid arthritis, periodontitis and the aseptic loosening of orthopedic implants. Thus, identification of agents that can suppress osteoclast formation and bone resorption is important for the treatment of these diseases. Monocrotaline (Mon), the major bioactive component of crotalaria sessiliflora has been investigated for its anti-cancer activities. However, the effect of Mon on osteoclast formation and osteolysis is not known. Methods: The bone marrow macrophages (BMMs) were cultured with M-CSF and RANKL followed by Mon treatment. Then the effects of Mon on osteoclast differentiation were evaluated by counting TRAP (+) multinucleated cells. Moreover, effects of Mon on hydroxyapatite resorption activity of mature osteoclast were studied through resorption areas measurement. The involved potential signaling pathways were analyzed by performed Western blotting and quantitative real-time PCR examination. Further, we established a mouse calvarial osteolysis model to measure the osteolysis suppressing effect of Mon in vivo. Results: In this study, we show that Mon can inhibit RANKL-induced osteoclast formation and function in a dose-dependent manner. Mon inhibits the expression of osteoclast marker genes such as tartrate-resistant acid phosphatase (TRAP) and cathepsin K. Furthermore, Mon inhibits RANKL-induced the activation of p38 and JNK. Consistent with in vitro results, Mon exhibits protective effects in an in vivo mouse model of LPS-induced calvarial osteolysis. Conclusion: Taken together our data demonstrate that Mon may be a potential prophylactic anti-osteoclastic agent for the treatment of osteolytic diseases caused by excessive osteoclast formation and function.

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Artesunate inhibits RANKL‐induced osteoclastogenesis and bone resorption in vitro and prevents LPS‐induced bone loss in vivo

Cited by 41 publications

References 38 publications

Asperpyrone A attenuates RANKL‐induced osteoclast formation through inhibiting NFATc1, Ca²⁺ signalling and oxidative stress

Asperpyrone A attenuates RANKL‐induced osteoclast formation through inhibiting NFATc1, Ca²⁺ signalling and oxidative stress

Ligustilide suppresses RANKL‐induced osteoclastogenesis and bone resorption via inhibition of RANK expression

Monocrotaline Suppresses RANKL-Induced Osteoclastogenesis In Vitro and Prevents LPS-Induced Bone Loss In Vivo

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Artesunate inhibits RANKL‐induced osteoclastogenesis and bone resorption in vitro and prevents LPS‐induced bone loss in vivo

Cited by 41 publications

References 38 publications

Asperpyrone A attenuates RANKL‐induced osteoclast formation through inhibiting NFATc1, Ca2+ signalling and oxidative stress

Asperpyrone A attenuates RANKL‐induced osteoclast formation through inhibiting NFATc1, Ca2+ signalling and oxidative stress

Ligustilide suppresses RANKL‐induced osteoclastogenesis and bone resorption via inhibition of RANK expression

Monocrotaline Suppresses RANKL-Induced Osteoclastogenesis In Vitro and Prevents LPS-Induced Bone Loss In Vivo

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Asperpyrone A attenuates RANKL‐induced osteoclast formation through inhibiting NFATc1, Ca²⁺ signalling and oxidative stress

Asperpyrone A attenuates RANKL‐induced osteoclast formation through inhibiting NFATc1, Ca²⁺ signalling and oxidative stress