Chrysophanic acid shifts the differentiation tendency of BMSCs to prevent alcohol‐induced osteonecrosis of the femoral head

Yu, Hongping; Liu, Pei; Zhu, Daoyu; Yin, Junhui; Yang, Qianhao; Huang, Yigang; Chen, Yixuan; Zhang, Changqing; Gao, You-Shui

doi:10.1111/cpr.12871

Cited by 19 publications

(17 citation statements)

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“…Therefore, BMSCs are the key factor for the development and treatment of alcoholic ONFH. In the present study, ethanol significantly inhibited the proliferation and osteogenic differentiation of BMSCs, which was consistent with our previous research 21,26 . Moreover, Alda‐1 could obviously reverse the inhibition of ethanol‐induced proliferation and osteogenic differentiation of BMSCs.…”

Section: Discussionsupporting

confidence: 92%

“…Our results also demonstrated that ethanol significantly promoted the adipogenic differentiation, fortunately, Alda‐1 significantly retarded alcohol‐induced adipogenesis of BMSCs via AMPK pathway. Our previous studies indicated that ethanol promoted adipogenesis leading to ONFH by AMPK pathway 21 . Moreover, Alda‐1 activation of ALDH 2 protected against ethanol‐induced cardiac defect and apoptosis via AMPK signalling 30 .…”

Section: Discussionmentioning

confidence: 96%

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Activation of aldehyde dehydrogenase 2 protects ethanol‐induced osteonecrosis of the femoral head in rat model

et al. 2022

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Objectives: Osteonecrosis of the femoral head (ONFH) is a devastating disease characterized by destructive bone structures, enlarged adipocyte accumulation and impaired vascularization. The aldehyde dehydrogenase 2 (ALDH 2) is the limiting enzyme for ethanol metabolism with many physiological functions. The aim was investigated the potential protective role of activated ALDH 2 by Alda-1 for ethanolinduced ONFH. Materials and Methods:The ethanol-induced ONFH in rat was performed to explore the protective of Alda-1 by various experimental methods. Subsequently, the effect of Alda-1 and ethanol on the osteogenic and adipogenic differentiation was investigated via multiple cellular and molecular methods. Finally, the effect of Alda-1 and ethanol on the neo-vascularization was detected in Human umbilical vein endothelial cells (HUVECs) and ONFH model.Results: Firstly, radiographical and pathological measurements indicated that alda-1 protected ethanol-induced ONFH. Moreover, ethanol significantly inhibited the proliferation and osteogenic differentiation of BMSCs, whereas Alda-1 could distinctly rescue it by PI3K/AKT signalling. Secondly, ethanol remarkably promoted the lipid vacuoles formation of BMSCs, while Alda-1 significantly retarded it on BMSCs by AMPK signalling pathway. Finally, ethanol significantly inhibited proliferation and growth factor level resulting in reduced angiogenesis, whereas Alda-1 could rescue the effect of ethanol. Additionally, Alda-1 significantly reduced the occurrence of ONFH and promoted vessel number and distribution in alcoholic ONFH.Conclusions: Alda-1 activation of ALDH 2 was highly demonstrated to protect ethanol-induced ONFH by triggering new bone formation, reducing adipogenesis and stimulating vascularization.Xiaoyi Lin and Daoming Zhu are co-first authors and contributed equally to this work.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 96%

Activation of aldehyde dehydrogenase 2 protects ethanol‐induced osteonecrosis of the femoral head in rat model

et al. 2022

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“…In recent years, traditional Chinese medicines (TCMs) show obvious therapeutic effects and advantages in many disease treatments [ 5 , 6 ]. For instance, andrographolide alleviates oxidative stress and inflammation in arthritis [ 7 ], flavonoids promote bone repair in COM [ 8 ], and betulinic acid relieves synovial inflammation in arthritis [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

Network Pharmacology-Based Analysis on Lonicera japonica for Chronic Osteomyelitis Treatment

Shao

Huang

2022

Journal of Oncology

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Ethnopharmacological Relevance. Lonicera japonica (LJP) is a broadly used traditional Chinese medication treatment for chronic osteomyelitis (COM). But, the main antiosteomyelitis compounds and functional targets of LJP are still unclear. Aim of the Study. To screen LJP drug targets and active compounds in COM treatment. Materials and Methods. Active compounds of LJP were examined established on the analysis platform, Traditional Chinese Medicine Systems Pharmacology (TCMSP) database. DrugBank identified drug targets and annotated them on UniPort and GeneCards. Besides, the COM-related genes were identified on GeneCards. The network of the drug, main active compounds, targets, and diseases was built utilizing Cytoscape. STRING was utilized to build the protein-protein interaction network. Moreover, the KEGG and GO pathway enrichment analysis were applied to analyze biological function. Results. 23 active compounds of LJP were screened, and 204 drug targets and 686 COM-related genes were identified. Forty-five intersection genes were overlapped from 204 drug targets and 686 COM-related genes. The drug-active compounds-target protein-diseases network was established based on 23 active compounds of LJP and 45 intersection genes. Moreover, the interaction of 45 intersection genes was explored by the PPI network, and the drug-active compounds-target protein-diseases network was formed grounded by 23 active compounds of LJP, 45 intersection genes, and PPI network. The KEGG and GO pathway enrichment analysis specified that 45 intersection genes primarily enriched in immune-related pathways and oxidative stress-related pathways. Conclusions. In the research done, the main active compounds of LJP and drug targets in the treatment of COM were identified. Our findings might provide the ingredient option of LJP and drug targets of LJP in COM treatment.

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“…It has been reported that alcohol can destroy bone homeostasis by directly inhibiting the proliferation and differentiation of bone marrow mesenchymal stem cells (BMSCs). 3 In particularly, alcohol significantly inhibited the proliferation and DNA synthesis of osteoprogenitor cells. 4 Therefore, alcohol is a factor that cannot be ignored to cause osteonecrosis of the femoral head.…”

Section: Introductionmentioning

confidence: 95%

“…9 RAB40C, also known as RARL/RASL8C, is located in 16p13. 3. It is a member of the RAS oncogene family and encodes the protein RAB40C.…”

Section: Introductionmentioning

confidence: 99%

RAB40C Gene Polymorphisms Were Associated with Alcohol-Induced Osteonecrosis of the Femoral Head

Liu¹,

Li²,

Li³

2021

IJGM

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Introduction: Alcohol-induced osteonecrosis of the femoral head (ONFH), a progressive disease, is caused by excessive drinking and genetic factors. Currently, it remains to represent a significant challenge. The association between alcohol-induced ONFH and RAB40C gene polymorphisms may provide a direction for the mechanism of alcoholic ONFH. Methods: A total of 201 alcohol-induced ONFH patients and 201 healthy controls were recruited in this case-control study. The polymorphisms of RAB40C gene were genotyped in blood samples by Agena MassARRAY RS1000. Pearson chi-square test was used to calculate difference in allele frequencies of gene polymorphisms between the cases and controls. Alcohol-induced ONFH risk was estimated using odds ratios (ORs) and 95% confidence intervals (CIs). Results: In the overall analysis, the allele "G" of rs62030917 was significantly increased alcohol-induced ONFH risk (OR = 1.47, 95% CI = 1.07-2.02, p = 0.017) in the allele model. In the genetic analysis, rs62030917 also increased the risk of alcohol-induced ONFH in the dominant model (adjusted OR = 1.52, 95% CI=1.02-2.26, p = 0.039) and the log-additive model (adjusted OR = 1.42, 95% CI=1.05-1.93, p = 0.025). Age stratification analysis suggested that rs62030917 increased the risk of alcohol-induced ONFH among the individuals younger than 42 years old. Moreover, carriers of AA, GA and GG genotypes in rs2269556 had LDL-C levels that were significantly different (p = 0.047). Among them, carriers of GG genotype had the highest LDL-C levels. Conclusion:This study revealed rs62030917 in RAB40C gene might increase the risk of alcohol-induced ONFH, providing a theoretical basis for the mechanism of RAB40C in alcohol-induced ONFH.

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Chrysophanic acid shifts the differentiation tendency of BMSCs to prevent alcohol‐induced osteonecrosis of the femoral head

Cited by 19 publications

References 50 publications

Activation of aldehyde dehydrogenase 2 protects ethanol‐induced osteonecrosis of the femoral head in rat model

Activation of aldehyde dehydrogenase 2 protects ethanol‐induced osteonecrosis of the femoral head in rat model

Network Pharmacology-Based Analysis on Lonicera japonica for Chronic Osteomyelitis Treatment

RAB40C Gene Polymorphisms Were Associated with Alcohol-Induced Osteonecrosis of the Femoral Head

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