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Research
siqian wang
The school and hospital of wenzhou medical university
Corresponding Author
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Background: Iron overload is common in patients with haematological disorders, and it is known to have a suppressive effect on haematogenesis. However, the mechanism by which iron overload affects haematogenesis is still unclear. The antioxidant curcumin has been reported to protect against iron overload-induced bone marrow damage, although the mechanism underlying this protective effect remains to be elucidated.
Methods: We established iron overload cell and mouse models. Mitochondrion-derived reactive oxygen species (mROS) levels, autophagy levels, and the SIRT3/SOD2 pathway were examined in these models and in the bone marrow of patients with iron overload.
Results: Iron overload was shown to depress haematogenesis and induce mitochondrion-derived superoxide anion-dependent autophagic cell death. Iron loading decreased SIRT3 protein expression, promoted an increase in SOD2, and led to the elevation of mROS. These effects were reversed by the overexpression of SIRT3. Curcumin treatment ameliorated peripheral blood cells, enhanced SIRT3 activity, decreased SOD2 acetylation, inhibited mROS production, and suppressed iron loading-induced autophagy.
Conclusions: These results suggest that curcumin exerts a protective effect on bone marrow by reducing mROS-stimulated autophagic cell death in a manner dependent on the SIRT3/SOD2 pathway.
Keywords
curcumin, iron overload, bone marrow damage, autophagy, mitochondrial ROS
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
siqian wang
The school and hospital of wenzhou medical university
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
View the published article at Cellular & Molecular Biology Letters.
Version 1
Posted 12 Jun, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Hematology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Cellular & Molecular Biology Letters.
Background: Iron overload is common in patients with haematological disorders, and it is known to have a suppressive effect on haematogenesis. However, the mechanism by which iron overload affects haematogenesis is still unclear. The antioxidant curcumin has been reported to protect against iron overload-induced bone marrow damage, although the mechanism underlying this protective effect remains to be elucidated.
Methods: We established iron overload cell and mouse models. Mitochondrion-derived reactive oxygen species (mROS) levels, autophagy levels, and the SIRT3/SOD2 pathway were examined in these models and in the bone marrow of patients with iron overload.
Results: Iron overload was shown to depress haematogenesis and induce mitochondrion-derived superoxide anion-dependent autophagic cell death. Iron loading decreased SIRT3 protein expression, promoted an increase in SOD2, and led to the elevation of mROS. These effects were reversed by the overexpression of SIRT3. Curcumin treatment ameliorated peripheral blood cells, enhanced SIRT3 activity, decreased SOD2 acetylation, inhibited mROS production, and suppressed iron loading-induced autophagy.
Conclusions: These results suggest that curcumin exerts a protective effect on bone marrow by reducing mROS-stimulated autophagic cell death in a manner dependent on the SIRT3/SOD2 pathway.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
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