Catalpol protects against 2,3,7,8‐tetrachlorodibenzo‐<i>p</i>‐dioxin‐induced cytotoxicity in osteoblastic MC3T3‐E1 cells

Choi, Eun Mi; Suh, Kwang Sik; Jung, Woon‐Won; Yun, Soojin; Park, So Young; Chin, Sang Ouk; Rhee, Sang Youl; Chon, Suk

doi:10.1002/jat.3896

Cited by 11 publications

(6 citation statements)

References 49 publications

(71 reference statements)

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“…CA has been reported to alleviate oxidative stress through upregulation of antioxidant enzymes in animal models of diabetes. , The current study revealed that CA partially suppressed the upregulation of ROS levels in MC3T3-E1 cells on the surface of titanium plates under HGHL conditions, subsequently leading to enhanced osteogenesis of MC3T3-E1 cells (Figure ). Consistent with our findings, Choi et al demonstrated that CA had the potential to mitigate the toxicity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in MC3T3-E1 cells due to its antioxidant properties . These findings led us to hypothesize that CA partially abrogates the damage caused by HGHL-induced oxidative stress in osteoblasts.…”

Section: Discussionsupporting

confidence: 91%

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Catalpol Promotes Osseointegration of Titanium Implants under Conditions of Type 2 Diabetes via AKT/GSK3β/FYN Pathway-Mediated NRF2 Activation

Zhang,

Sun

et al. 2024

ACS Omega

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Catalpol (CA), a compound derived from the roots of Rehmannia glutinosa, is recognized for its anti-oxidative and antiinflammatory properties. The current study aimed to evaluate the impact of CA on the osseointegration of titanium implants (TIs) in the context of type 2 diabetes and elucidate the underlying pharmacological mechanisms. MC3T3-E1 cells were incubated on the surface of titanium plates and exposed to various media for investigating osteoblast behaviors, as follows: regular medium, medium of high glucose and high lipid (HGHL) that simulates diabetic conditions, HGHL + CA medium, or HGHL + CA + LY294002 (an inhibitor of phosphoinositide 3-kinase or PI3K) medium. TIs were also surgically implanted into the femoral condyle defects in normal mice and mouse models of type 2 diabetes mellitus (T2DM). HGHL-induced oxidative stress was found to cause osteoblast dysfunction, accompanied by the inactivation of AKT/GSK3β/FYN pathway-mediated NRF2 signaling. However, CA administration effectively mitigated HGHL-induced oxidative stress and reactivated AKT/GSK3β/FYN/NRF2 signaling, resulting in the reversal of HGHL-induced dysfunctions in MC3T3-E1 cells, as evidenced by enhanced osteoblast adhesion, proliferation, and differentiation, as well as reduced apoptotic injury. In addition, the positive effects of CA were confirmed in vivo by enhanced osseointegration of TIs observed in mouse models of T2DM using microcomputed tomography and histological analyses. However, the pro-osteogenic effects of CA were almost completely nullified by the addition of LY294002. These findings demonstrated for the first time that CA administration ameliorates the impairment in osseointegration of TIs under conditions of T2DM via AKT/GSK3β/FYN pathway-mediated NRF2 activation. Given its antioxidative and pro-osteogenic properties, CA administration holds promise as a reliable therapeutic strategy in the future for implant restoration in patients with T2DM.

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Section: Discussionsupporting

confidence: 91%

“…Consistent with our findings, Choi et al demonstrated that CA had the potential to mitigate the toxicity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in MC3T3-E1 cells due to its antioxidant properties. 33 These findings led us to hypothesize that CA partially abrogates the damage caused by HGHL-induced oxidative stress in osteoblasts.…”

Section: Discussionmentioning

confidence: 99%

Catalpol Promotes Osseointegration of Titanium Implants under Conditions of Type 2 Diabetes via AKT/GSK3β/FYN Pathway-Mediated NRF2 Activation

Zhang,

Sun

et al. 2024

ACS Omega

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“…Catalpol, an iridoid glycoside isolated from the roots of R. glutinosa, has been reported to display neuroprotective effects (38,39). Previous studies have also demonstrated the cardioprotective and anti-inflammatory properties of catalpol, including apoptosis inhibition, reduced neuronal death and promotion of differentiation (40,41). In a mouse model of lipopolysaccharide-induced acute lung injury, catalpol prevents injury by inhibiting TNF-α, IL-1β and IL-6 expression (42).…”

Section: Discussionmentioning

confidence: 99%

Catalpol ameliorates doxorubicin‑induced inflammation and oxidative stress in H9C2 cells through PPAR‑γ activation

Jiang

Zhang

2020

Exp Ther Med

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Drug-induced cardiomyopathy is a severe disease that leads to refractory heart disease at late stages, with increasing detrimental effects. DOX-induced cell damage is primarily induced via cellular oxidative stress. The present study investigated the effects of catalpol on doxorubicin (DOX)-induced H9C2 cardiomyocyte inflammation and oxidative stress. The Cell Counting Kit-8 assay was performed to detect cell viability, and western blotting was performed to detect the expression of peroxisome proliferator-activated receptor (PPAR)-γ in H9C2 cells. The expression levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 were measured using ELISAs. Furthermore, the oxidative stress kit was used to detect the levels of malondialdehyde, superoxide dismutase and glutathione peroxidase. A reactive oxygen species (ROS) kit and DCF-DA staining were used to detect ROS levels. The results indicated that DOX treatment inhibited H9C2 cell expression of PPAR-γ and decreased H9C2 cell viability. Various concentrations of catalpol exhibited a less potent effect on H9C2 cell viability compared with DOX; however, catalpol increased the viability of DOX-induced H9C2 cells. Catalpol treatment also significantly decreased the expression levels of inflammatory factors (TNF-α, IL-1β and IL-6) in DOX-induced H9C2 cells, which was reversed by transfections with short hairpin RNA targeting PPAR-γ. Results from the present study indicated that catalpol ameliorated DOX-induced inflammation and oxidative stress in H9C2 cardiomyoblasts by activating PPAR-γ.

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“…Their work was further validated by the study from Cheng et al, which demonstrated that catalpol could enhance the activity of Wnt/β-catenin axis in MC3T3-E1 osteoblasts under high glucose condition [34]. Choi et al also reported that catalpol prevents MC3T3-E1 osteoblasts apoptosis caused by TCDD-induced damage [35]. Lai and his colleagues found that catalpol could alleviate bone loss by mediating the Th1/Th2 cells paradigm [36].…”

Section: Discussionmentioning

confidence: 92%

STAT3 activation by catalpol promotes osteogenesis-angiogenesis coupling, thus accelerating osteoporotic bone repair

et al. 2021

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Background Bone fracture repair has gained a lot of attention due to the high incidence of delayed union or even nonunion especially in osteoporotic patients, resulting in a dreadful impact on the quality of life. However, current therapies involve the costly expense and hence become unaffordable strategies for fracture recovery. Herein, developing new strategies for better bone repair is essential and urgent. Catalpol treatment has been reported to attenuate bone loss and promote bone formation. However, the mechanisms underlying its effects remain unraveled. Methods Rat bone marrow mesenchymal stem cells (BMSCs) were isolated from rat femurs. BMSC osteogenic ability was assessed using ALP and ARS staining, immunofluorescence, and western blot analysis. BMSC-mediated angiogenic potentials were determined using the western blot analysis, ELISA testing, scratch wound assay, transwell migration assay, and tube formation assay. To investigate the molecular mechanism, the lentivirus transfection was used. Ovariectomized and sham-operated rats with calvaria defect were analyzed using micro-CT, H&E staining, Masson’s trichrome staining, microfil perfusion, sequential fluorescent labeling, and immunohistochemistry assessment after administrated with/without catalpol. Results Our results manifested that catalpol enhanced BMSC osteoblastic differentiation and promoted BMSC-mediated angiogenesis in vitro. More importantly, this was conducted via the JAK2/STAT3 pathway, as knockdown of STAT3 partially abolished beneficial effects in BMSCs. Besides, catalpol administration facilitated bone regeneration as well as vessel formation in an OVX-induced osteoporosis calvarial defect rat model. Conclusions The data above showed that catalpol could promote osteogenic ability of BMSC and BMSC-dependent angiogenesis through activation of the JAK2/STAT3 axis, suggesting it may be an ideal therapeutic agent for clinical medication of osteoporotic bone fracture.

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Catalpol protects against 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin‐induced cytotoxicity in osteoblastic MC3T3‐E1 cells

Cited by 11 publications

References 49 publications

Catalpol Promotes Osseointegration of Titanium Implants under Conditions of Type 2 Diabetes via AKT/GSK3β/FYN Pathway-Mediated NRF2 Activation

Catalpol Promotes Osseointegration of Titanium Implants under Conditions of Type 2 Diabetes via AKT/GSK3β/FYN Pathway-Mediated NRF2 Activation

Catalpol ameliorates doxorubicin‑induced inflammation and oxidative stress in H9C2 cells through PPAR‑γ activation

STAT3 activation by catalpol promotes osteogenesis-angiogenesis coupling, thus accelerating osteoporotic bone repair

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