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Research article
Dae Yu Kim
Corresponding Author
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Background: Oxidative damage in retinal pigmented epithelium (RPE) cells contributes to the development of age-related macular degeneration, which is among the leading causes of visual loss in elderly people. In the present study, we evaluated the protective role of TPP-Niacin against the hydrogen peroxide (H2O2)-induced oxidative stress to RPE cells.
Methods: The cellular viability, lactate dehydrogenase, reactive oxygen species (ROS), and mitochondrial function were determined in the retinal ARPE-19 cells under the treatment with H2O2 or pre-treatment with TPP-Niacin. The expression level of mitochondrial related genes and some transcription factors were assessed using real-time polymerase chain reaction (RT-PCR).
Results: TPP-Niacin significantly improved cell viability reduction, reduced ROS generation and increased the antioxidant enzymes in H2O2-treated ARPE-19 cells. Mitochondrial dysfunction from H2O2-induced oxidative stress was also significantly diminished by the TPP-Niacin treatment, reduced generation of ROS, an ameliorated reduction of mitochondrial membrane potential (MMP) and an upregulated mitochondrial associated gene. In addition, TPP-Niacin markedly enhanced the expression of transcription factors (PGC-1α and NRF2) and antioxidant associated genes (especially, HO-1 and NQO-1).
Conclusion: We proved the protective effect of TPP-Niacin against H2O2-induced oxidative stress in RPE cells. TPP-Niacin is believed to have played a protective role against mitochondrial dysfunction by up-regulating antioxidant-related genes such as PGC-1α, NRF2, HO-1 and NQO-1 in RPE cells.
Keywords
age-related macular degeneration, retinal pigment epithelium, mitochondrial function, antioxidants
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CURRENT STATUS: Published
View the published article at BMC Pharmacology and Toxicology.
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Editorial decision: Accept
On 23 Dec, 2020
Reviewer #1 agreed
On 21 Dec, 2020
Review #1 received
Received 21 Dec, 2020
Reviewers invited
Invitations sent on 20 Dec, 2020
Editor assigned
On 19 Dec, 2020
Submission checks complete
On 19 Dec, 2020
Editor invited
On 19 Dec, 2020
No comments provided
Editorial decision: Minor revision
On 06 Dec, 2020
Review #2 received
Received 05 Dec, 2020
Reviewer #2 agreed
On 22 Nov, 2020
Review #1 received
Received 11 Nov, 2020
Reviewer #1 agreed
On 09 Nov, 2020
Reviewers invited
Invitations sent on 02 Nov, 2020
Editor assigned
On 01 Nov, 2020
Submission checks complete
On 01 Nov, 2020
Editor invited
On 01 Nov, 2020
Version 1
Posted 26 Jun, 2020
No comments provided
Editorial decision: Major revision
On 06 Oct, 2020
Review #2 received
Received 02 Oct, 2020
Reviewer #2 agreed
On 08 Sep, 2020
Review #1 received
Received 08 Sep, 2020
Reviewer #1 agreed
On 20 Aug, 2020
Reviewers invited
Invitations sent on 26 Jun, 2020
Editor invited
On 25 Jun, 2020
Editor assigned
On 25 Jun, 2020
Submission checks complete
On 24 Jun, 2020
First submitted
On 21 Jun, 2020
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See the published version of this preprint at BMC Pharmacology and Toxicology.
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.
Learn more about In Review
Research article
Dae Yu Kim
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at BMC Pharmacology and Toxicology.
No community comments so far
Editorial decision: Accept
On 23 Dec, 2020
Reviewer #1 agreed
On 21 Dec, 2020
Review #1 received
Received 21 Dec, 2020
Reviewers invited
Invitations sent on 20 Dec, 2020
Editor assigned
On 19 Dec, 2020
Submission checks complete
On 19 Dec, 2020
Editor invited
On 19 Dec, 2020
No comments provided
Editorial decision: Minor revision
On 06 Dec, 2020
Review #2 received
Received 05 Dec, 2020
Reviewer #2 agreed
On 22 Nov, 2020
Review #1 received
Received 11 Nov, 2020
Reviewer #1 agreed
On 09 Nov, 2020
Reviewers invited
Invitations sent on 02 Nov, 2020
Editor assigned
On 01 Nov, 2020
Submission checks complete
On 01 Nov, 2020
Editor invited
On 01 Nov, 2020
Version 1
Posted 26 Jun, 2020
No comments provided
Editorial decision: Major revision
On 06 Oct, 2020
Review #2 received
Received 02 Oct, 2020
Reviewer #2 agreed
On 08 Sep, 2020
Review #1 received
Received 08 Sep, 2020
Reviewer #1 agreed
On 20 Aug, 2020
Reviewers invited
Invitations sent on 26 Jun, 2020
Editor invited
On 25 Jun, 2020
Editor assigned
On 25 Jun, 2020
Submission checks complete
On 24 Jun, 2020
First submitted
On 21 Jun, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Pharmacology and Toxicology.
Background: Oxidative damage in retinal pigmented epithelium (RPE) cells contributes to the development of age-related macular degeneration, which is among the leading causes of visual loss in elderly people. In the present study, we evaluated the protective role of TPP-Niacin against the hydrogen peroxide (H2O2)-induced oxidative stress to RPE cells.
Methods: The cellular viability, lactate dehydrogenase, reactive oxygen species (ROS), and mitochondrial function were determined in the retinal ARPE-19 cells under the treatment with H2O2 or pre-treatment with TPP-Niacin. The expression level of mitochondrial related genes and some transcription factors were assessed using real-time polymerase chain reaction (RT-PCR).
Results: TPP-Niacin significantly improved cell viability reduction, reduced ROS generation and increased the antioxidant enzymes in H2O2-treated ARPE-19 cells. Mitochondrial dysfunction from H2O2-induced oxidative stress was also significantly diminished by the TPP-Niacin treatment, reduced generation of ROS, an ameliorated reduction of mitochondrial membrane potential (MMP) and an upregulated mitochondrial associated gene. In addition, TPP-Niacin markedly enhanced the expression of transcription factors (PGC-1α and NRF2) and antioxidant associated genes (especially, HO-1 and NQO-1).
Conclusion: We proved the protective effect of TPP-Niacin against H2O2-induced oxidative stress in RPE cells. TPP-Niacin is believed to have played a protective role against mitochondrial dysfunction by up-regulating antioxidant-related genes such as PGC-1α, NRF2, HO-1 and NQO-1 in RPE cells.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
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