Poligoniï¿½Multiflori Radix enhances osteoblast formation and reduces osteoclast differentiation

Han, Sang‐Yong; Lee, Kyung‐Hee; Kim, Yun‐Kyung

doi:10.3892/ijmm.2018.3603

Cited by 5 publications

(9 citation statements)

References 46 publications

(47 reference statements)

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“…NFATc1 is a member of the NFAT transcription superfamily and a master transcription factor in RANKL-induced osteoclastogenesis that regulates the expression of osteoclast-specific genes (Han, Lee, & Kim, 2018;Ranjan et al, 2014). Our results show that morin effec- In addition, NFATc1 is regulated by the MAPK signalling pathway, especially ERK and p38.…”

Section: Discussionmentioning

confidence: 69%

“…NFATc1 is a member of the NFAT transcription superfamily and a master transcription factor in RANKL‐induced osteoclastogenesis that regulates the expression of osteoclast‐specific genes (Han, Lee, & Kim, 2018; Ranjan et al, 2014). Our results show that morin effectively downregulated osteoclast differentiation and bone absorption in primary bone marrow‐derived osteoclasts by attenuating the expression of NFATc1, which is a major regulator of osteoclast differentiation (Q. Wang et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

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Morin attenuates osteoclast formation and function by suppressing the NF‐κB, MAPK and calcium signalling pathways

Shi

Shen

et al. 2021

Phytotherapy Research

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Morin is a natural compound isolated from moraceae family members and has been reported to possess a range of pharmacological activities. However, the effects of morin on bone-associated disorders and the potential mechanism remain unknown.In this study, we investigated the anti-osteoclastogenic effect of morin in vitro and the potential therapeutic effects on ovariectomy (OVX)-induced osteoporosis in vivo.In vitro, by using a bone marrow macrophage-derived osteoclast culture system, we determined that morin attenuated receptor activator of nuclear factor (NF)-κB ligand (RANKL)-induced osteoclast formation via the inhibition of the mitogen-activated protein kinase (MAPK), NF-κB and calcium pathways. In addition, the subsequent expression of nuclear factor of activated T cells c1 (NFATc1) and c-fos was significantly suppressed by morin. In addition, NFATc1 downregulation led to the reduced expression of osteoclastogenesis-related marker genes, such as V-ATPase-d2 and Integrin β3. In vivo, results provided that morin could effectively attenuate OVXinduced bone loss in C57BL/6 mice. In conclusion, our results demonstrated that morin suppressed RANKL-induced osteoclastogenesis via the NF-κB, MAPK and calcium pathways, in addition, its function of preventing OVX-induced bone loss in vivo, which suggested that morin may be a potential therapeutic agent for postmenopausal osteoporosis treatment.

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Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Morin attenuates osteoclast formation and function by suppressing the NF‐κB, MAPK and calcium signalling pathways

Shi

Shen

et al. 2021

Phytotherapy Research

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“…Experimental durations less than 2 weeks generally consisted of two to three injections of LPS ranging from 5 to 10 mg/kg body weight per injection with bones collected for ex vivo analysis within 2 weeks of the first LPS exposure. This type of experimental design consistently demonstrated negative effects of LPS on trabecular bone structure, including BV/TV, Tb.N, and Tb.Sp, in the femur ( 42‐118 ) and tibia. ( 68,119‐124 ) In studies that reported negative effects of LPS exposure on trabecular bone structure, approximately half (22/47) also reported a decreased Tb.Th in the femur ( 48,55,59,70,77,81,88,89,94,97‐101,107,108,114,117,123 ) and tibia.…”

Section: Resultsmentioning

confidence: 99%

Lipopolysaccharide-Induced Bone Loss in Rodent Models: A Systematic Review and Meta-Analysis

Bott

Feldman

Comelli

et al. 2020

Journal of Bone and Mineral Research

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Osteoporosis has traditionally been characterized by underlying endocrine mechanisms, though evidence indicates a role of inflammation in its pathophysiology. Lipopolysaccharide (LPS), a component of gram‐negative bacteria that reside in the intestines, can be released into circulation and stimulate the immune system, upregulating bone resorption. Exogenous LPS is used in rodent models to study the effect of systemic inflammation on bone, and to date a variety of different doses, routes, and durations of LPS administration have been used. The study objective was to determine whether systemic administration of LPS induced inflammatory bone loss in rodent models. A systematic search of Medline and four other databases resulted in a total of 110 studies that met the inclusion criteria. Pooled standardized mean differences (SMDs) and corresponding 95% confidence intervals (CI) with a random‐effects meta‐analyses were used for bone volume fraction (BV/TV) and volumetric bone mineral density (vBMD). Heterogeneity was quantified using the I2 statistic. Shorter‐term (<2 weeks) and longer‐term (>2 weeks) LPS interventions were analyzed separately because of intractable study design differences. BV/TV was significantly reduced in both shorter‐term (SMD = −3.79%, 95% CI [−4.20, −3.38], I2 62%; p < 0.01) and longer‐term (SMD = −1.50%, 95% CI [−2.00, −1.00], I2 78%; p < 0.01) studies. vBMD was also reduced in both shorter‐term (SMD = −3.11%, 95% CI [−3.78, −2.44]; I2 72%; p < 0.01) and longer‐term (SMD = −3.49%, 95% CI [−4.94, −2.04], I2 82%; p < 0.01) studies. In both groups, regardless of duration, LPS negatively impacted trabecular bone structure but not cortical bone structure, and an upregulation in bone resorption demonstrated by bone cell staining and serum biomarkers was reported. This suggests systemically delivered exogenous LPS in rodents is a viable model for studying inflammatory bone loss, particularly in trabecular bone. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).

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“…In addition, we analyzed the expression of osteoblast-specific markers, such as ALP, RANKL, and osteocalcin (OCN). As shown in Supplemental Figure S3 , NAPMA treatment did not influence the expression of osteoblast differentiation ( Supplemental Figure S3A ), ALP activity ( Supplemental Figure S3B ), and differentiation markers ALP, RANKL, and osteocalcin ( Supplemental Figure S3C ) [ 25 ].…”

Section: Resultsmentioning

confidence: 99%

N-[2-(4-Acetyl-1-Piperazinyl)Phenyl]-2-(3-Methylphenoxy)Acetamide (NAPMA) Inhibits Osteoclast Differentiation and Protects against Ovariectomy-Induced Osteoporosis

et al. 2020

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Osteoclasts are large, multinucleated cells responsible for bone resorption and are induced in response to the regulatory activity of receptor activator of nuclear factor-kappa B ligand (RANKL). Excessive osteoclast activity causes pathological bone loss and destruction. Many studies have investigated molecules that specifically inhibit osteoclast activity by blocking RANKL signaling or bone resorption. In recent years, we screened compounds from commercial libraries to identify molecules capable of inhibiting RANKL-induced osteoclast differentiation. Consequently, we reported some compounds that are effective at attenuating osteoclast activity. In this study, we found that N-[2-(4-acetyl-1-piperazinyl)phenyl]-2-(3-methylphenoxy)acetamide (NAPMA) significantly inhibited the formation of multinucleated tartrate-resistant acid phosphatase (TRAP)-positive cells from bone marrow-derived macrophages in a dose-dependent manner, without cytotoxic effects. NAPMA downregulated the expression of osteoclast-specific markers, such as c-Fos, NFATc1, DC-STAMP, cathepsin K, and MMP-9, at the transcript and protein levels. Accordingly, bone resorption and actin ring formation were decreased in response to NAPMA treatment. Furthermore, we demonstrated the protective effect of NAPMA against ovariectomy-induced bone loss using micro-CT and histological analysis. Collectively, the results showed that NAPMA inhibited osteoclast differentiation and attenuated bone resorption. It is thus a potential drug candidate for the treatment of osteoporosis and other bone diseases associated with excessive bone resorption.

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Poligoniï¿½Multiflori Radix enhances osteoblast formation and reduces osteoclast differentiation

Cited by 5 publications

References 46 publications

Morin attenuates osteoclast formation and function by suppressing the NF‐κB, MAPK and calcium signalling pathways

Morin attenuates osteoclast formation and function by suppressing the NF‐κB, MAPK and calcium signalling pathways

Lipopolysaccharide-Induced Bone Loss in Rodent Models: A Systematic Review and Meta-Analysis

N-[2-(4-Acetyl-1-Piperazinyl)Phenyl]-2-(3-Methylphenoxy)Acetamide (NAPMA) Inhibits Osteoclast Differentiation and Protects against Ovariectomy-Induced Osteoporosis

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