143
Views
3
CrossRef citations to date
0
Altmetric
Articles

Carnosol attenuates high glucose damage in human retinal endothelial cells through regulation of ERK/Nrf2/HO-1 pathway

ORCID Icon, ORCID Icon, ORCID Icon, ORCID Icon, & ORCID Icon
Pages 783-795 | Received 12 Apr 2022, Accepted 13 Oct 2022, Published online: 27 Oct 2022
 

Abstract

Carnosol is a natural compound with antioxidant properties. Based on this evidence, in the present study we investigated whether this compound can protect retinal vascular endothelium from hyperglycemic insult responsible for diabetic retinopathy development. We performed in vitro study on human retinal endothelial cells (HREC) cultured both in normal and high glucose conditions to assess the effects of carnosol on cell viability, Nrf2 expression, HO-1 activity, and ERK1/2 expression. HREC exposed to high glucose insult were treated with carnosol. Data indicated that carnosol treatment is able to induce HO-1 expression via Nrf2 activation and counteracts the damage elicited by high glucose. Further, carnosol activation of Nrf2/HO-1 signaling axis involves ERK1/2 pathway. These data confirm the therapeutic value of carnosol by suggesting its use to treat diabetic retinopathy.

Graphical Abstract

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was funded by Italian Ministry of Education, University and Research (MIUR) [grant number PRIN 2017TSHBXZ_003] and by the Grant PIano inCEntivi RIcerca (PIACERI) Ateneo 2020/2022 – Linea Intervento 2.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.