Role of Teriparatide in Glucocorticoid‐induced Osteoporosis through Regulating Cellular Reactive Oxygen Species

Wang, Tao; Han, Chao; Tian, Peng; Li, Pengfei; Ma, Xiaofang

doi:10.1111/os.12369

Cited by 19 publications

(20 citation statements)

References 26 publications

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“…Hodsman et al [54] stated that terparatide inhibit bone resorption by diminishing the number, function, and life span of osteoclasts. Wang et al [9] confirmed that teriparatide can diminish the level of the cellular ROS and stimulate osteocytes growth via triggering the protein kinase B (PKB) pathway. Meantime, the activated PKB can suppress caspase-3 proteolytic enzyme and stop the activation of apoptosis cascade.…”

Section: Discussionmentioning

confidence: 99%

“…Teriparatide enhances bone formation and subsequently bone resorption. It increase cortical bone thickness as well as trabecular bearing and interlink [9] . Wang et al [9] explained that teriparatide can diminish the level of the cellular ROS and stimulate osteocytes growth via triggering the protein kinase B (PKB) pathway Meantime, the activated PKB can suppress caspase-3 proteolytic enzyme and stop the activation of apoptosis cascade.…”

Section: Introductionmentioning

confidence: 94%

“…It increase cortical bone thickness as well as trabecular bearing and interlink [9] . Wang et al [9] explained that teriparatide can diminish the level of the cellular ROS and stimulate osteocytes growth via triggering the protein kinase B (PKB) pathway Meantime, the activated PKB can suppress caspase-3 proteolytic enzyme and stop the activation of apoptosis cascade. Teriparatide control the function of osteoblast via activation of the pathways signaling of cyclic AMP-dependent protein kinase A and calcium-dependent protein kinase C. It also triggers the MAP kinase and phospholipase A and D pathways [10] .…”

Section: Introductionmentioning

confidence: 94%

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Comparative Study on the Possible Protective Effect of Lepidium Sativum versus Teriparatide in Induced Osteoporosis in Adult Male Guinea Pigs

El-Haroun

Soliman

et al. 2020

Egyptian Journal of Histology

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Background: Osteoporosis is a major health problem. Teriparatide is a recombinant parathyroid hormone used as antiosteoporotic therapy. Lepidium sativum (LS) is widely used as a traditional herbal therapy for hypertension, diabetes and renal disorders. The LS seeds are widely known as a good traditional alternative medication for fracture healing.Objectives: Current research focused on evaluation of the Lepidium sativum versus teriparatide effect on glucocorticoidinduced osteoporosis Materials and Methods: 60 adult male guinea pigs were randomly divided into six equal groups: control groupI (distilled water); LS treated group (300 mg/kg suspended in distilled water orally by gastric tube), teriparatide treated group (4 mcg/ kg subcutaneously twice weekly), glucocorticoid treated group (3.5 mg/kg subcutaneously), teriparatide and glucocorticoids treated group and glucocorticoids and lepidium sativum treated group as pervious groups. At the end of the study, animals were anaesthetized and sacrificed. Femur bones of each animal were excised for histological and immunohistochemical studies (caspase-3 and osteoponotin). Results: Glucocorticoids induced bone resorption manifested as resorption cavities, thickened periosteum associated with decreased and irregular cortical and trabecular bone thickness. Marked reduced irregular collagen fibers were detected by trichrome staining. Immunohistochemically, this group showed positive immunoreactivity for caspase-3 in osteocytes and decrease in osteopontin deposits in bone matrix. Moreover, there was significant increase in number of osteoclasts associated with decrease in number of osteoblasts. Significant decrease in serum calcium level and increase in serum alkaline phosphatase were detected. Administration of either teriparatide or Lipidium sativum with glucocorticoids improved biochemical, histological and morphometric bone changes. They reduced osteocytes apoptosis and osteoclasts increase. Lipidium sativum was more effective improving changes induced by glucocorticoids. Conclusions: Glucocorticoids induced bone resorption. Despite the high cost of teriparatide, it did not achieve the desired protective effect. LS is cheap, available and its protective effect is promising with no adverse effects.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 94%

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Comparative Study on the Possible Protective Effect of Lepidium Sativum versus Teriparatide in Induced Osteoporosis in Adult Male Guinea Pigs

El-Haroun

Soliman

et al. 2020

Egyptian Journal of Histology

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“…Previous reports have shown that estrogen deficiency, a lack of exercise, and oxidative stress play a central role in the onset and development of postmenopausal osteoporosis 3,4 . Oxidative stress can produce excessive reactive oxygen species (ROS) and promote osteoblast damage [5][6][7] . Furthermore, ROS accelerates the apoptosis of osteoblasts, inhibiting their differentiation and impairing bone formation 8 .…”

Section: Introductionmentioning

confidence: 99%

Protection of Icariin Against Hydrogen Peroxide‐Induced MC3T3‐E1 Cell Oxidative Damage

Sun

Wang

2021

Orthopaedic Surgery

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Objective The aim of the present study was to evaluate the potential protective mechanism of icariin against oxidative damage caused by hydrogen peroxide in MC3T3‐E1 cells. Methods MC3T3‐E1 cells were treated with different concentrations of icariin to explore the optimal dose of icariin. MC3T3‐E1 cells were divided into groups treated with various concentrations of hydrogen peroxide (H2O2; 0, 0.1, 0.2, 0.5, 1, and 2 mM) for 24 h to induce oxidative damage and cell viability was assessed by Cell Counting Kit‐8 (CCK‐8) assay. Then, cells were divided into five groups: control, H2O2 (0.2 mM), icariin (0.1 μM) and H2O2 (0.2 mM), + icariin (0.1 μM). Cell viability was detected by CCK‐8 assay. In addition, the content of glutathione and superoxide dismutase and the activity level of malondialdehyde in these treatment groups were determined. Alkaline phosphatase (ALP) and alizarin red S (ARS) staining were also performed to measure the early and late osteogenesis, respectively. Protein expression of β‐catenin and cyclin D1 was measured by western blot assay. Then, we used an antagonist of Wnt/β‐catenin signaling pathway (DKK‐1) and western blot analysis to further explore potential mechanism. Results After 24 h of exposure to 0.2 mM H2O2, the viability of MC3T3‐E1 cells was significantly decreased compared to that of the control cells. We first found that icariin can promote cell proliferation of MC3T3‐E1 cells in a dose‐dependent manner, with the dosage 0.1 μM showing the best pro‐proliferative effect. Furthermore, icariin could promote the protein expression of OSX and RUNX2. The results showed that icariin can reverse the inhibitory osteogenic effects of MC3T3‐E1 caused by H2O2. In addition, icariin could increase the Wnt‐signaling related proteins. The results showed that MC3T3‐E1 cells in the H2O2 (0.2 mM) + icariin (0.1 μM) + Wnt‐signaling antagonist (DKK‐1) group had weaker ALP and ARS staining compared with that observed in the control and H2O2 (0.2 mM) + icariin (0.1 μM) groups. The ALP activity and calcium content were decreased in the 0.2 mM H2O2 + 0.1 μM icariin + DKK‐1 group compared to that observed in the 0.2 mM H2O2 + 0.1 μM icariin group. Conclusion The results showed that icariin can increase the viability of MC3T3‐E1 cells, reverse the oxidative stress induced by H2O2 and protect MC3T3‐E1 cells against H2O2‐induced inhibition of osteogenic differentiation, which may occur through the Wnt/β‐catenin signaling pathway.

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“…Next to neutrophils, an inhibition of intracellular ROS production after prednisolone and dexamethasone administration is also described for platelets [ 101 ]. However, in osteocyte-like cells, dexamethasone increased the ROS level compared to control groups [ 102 ]. These results underline the findings of the present study as prednisolone seemed to support pathogen killing, NET release and ROS production in certain dosages.…”

Section: Resultsmentioning

confidence: 99%

Methylprednisolone Induces Extracellular Trap Formation and Enhances Bactericidal Effect of Canine Neutrophils

Steffensen

Imker

Lassnig

et al. 2021

IJMS

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Methylprednisolone is a glucocorticoid and can negatively influence immune defense mechanisms. During bacterial infections in the dog, neutrophils infiltrate infected tissue and mediate antimicrobial effects with different mechanisms such as phagocytosis and neutrophil extracellular trap (NET) formation. Here, we investigated the influence of methylprednisolone on canine NET formation and neutrophil killing efficiency of Gram positive and Gram negative bacteria. Therefore, canine blood derived neutrophils were treated with different concentrations of methylprednisolone over time. The survival factor of Staphylococcus pseudintermedius, Streptococcus canis or Escherichia coli was determined in presence of stimulated neutrophils. Additionally, free DNA and nucleosomes as NET marker were analyzed in supernatants and neutrophils were assessed for NET formation by immunofluorescence microscopy. Methylprednisolone concentrations of 62.5 and 625 µg/mL enhanced the neutrophil killing of Gram positive bacteria, whereas no significant influence was detected for the Gram negative Escherichia coli. Interestingly, higher amounts of free DNA were detected under methylprednisolone stimulation in a concentration dependency and in the presence of Streptococcus canis and Escherichia coli. The nucleosome release by neutrophils is induced by bacterial infection and differs depending on the concentration of methylprednisolone. Furthermore, immunofluorescence microscopy analysis identified methylprednisolone at a concentration of 62.5 µg/mL as a NET inducer. In summary, methylprednisolone enhances NET-formation and time-dependent and concentration-dependent the bactericidal effect of canine neutrophils on Gram positive bacteria.

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Role of Teriparatide in Glucocorticoid‐induced Osteoporosis through Regulating Cellular Reactive Oxygen Species

Abstract: Teriparatide can reduce the cellular ROS level caused by glucocorticoids to facilitate the proliferation of osteocytes through activating the AKT pathway. Meanwhile, the activated AKT can inhibit the activity of proteolytic enzyme caspase-3 and prevent the activation of apoptosis cascade.

Cited by 19 publications

References 26 publications

Comparative Study on the Possible Protective Effect of Lepidium Sativum versus Teriparatide in Induced Osteoporosis in Adult Male Guinea Pigs

Comparative Study on the Possible Protective Effect of Lepidium Sativum versus Teriparatide in Induced Osteoporosis in Adult Male Guinea Pigs

Protection of Icariin Against Hydrogen Peroxide‐Induced MC3T3‐E1 Cell Oxidative Damage

Methylprednisolone Induces Extracellular Trap Formation and Enhances Bactericidal Effect of Canine Neutrophils

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