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Original Research Article | OPEN ACCESS

Autophagy inhibition by chloroquine prevents increase in blood pressure and preserves endothelial functions

Moon Jain1,2, Hina Iqbal3, Pankaj Yadav3, Himalaya Singh1,2, Debabrata Chanda3, Kumaravelu Jagavelu1,2, Kashif Hanif1,2

1Division of Pharmacology, Council of Scientific and Industrial Research-Central Drug Research Institute, Lucknow 226031, India; 2Academy of Scientific and Innovative Research, Ghaziabad, UP, India; 3Molecular Bioprospection Department, Council of Scientific and Industrial Research-Central Institute of Medicinal and Aromatic Plants, Lucknow 226015, India.

For correspondence:-  Kashif Hanif   Email: k_hanif@cdri.res.in   Tel:+915222772550

Accepted: 28 January 2020        Published: 30 April 2020

Citation: Jain M, Iqbal H, Yadav P, Singh H, Chanda D, Jagavelu K, et al. Autophagy inhibition by chloroquine prevents increase in blood pressure and preserves endothelial functions. Trop J Pharm Res 2020; 19(4):789-796 doi: 10.4314/tjpr.v19i4.16

© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To determine the effects of lysosomal inhibition of autophagy by chloroquine (CHQ) on hypertension-associated changes in the endothelial functions.
Method: Angiotensin II (Ang II)-treated human endothelial cell line EA.hy926 and renovascular hypertensive rats were subjected to CHQ treatment (in vitro: 0.5, 1, and 2.5 µM; in vivo: 50 mg/kg/day for three weeks). Changes in the protein expressions of LC3b II (autophagosome formation marker) and p62 (autophagy flux marker) were assessed using immunoblotting. Cell migration assay, tubule formation assay (in vitro), and organ bath studies (in vivo) were performed to evaluate the endothelial functions. Hemodynamic parameters were measured as well.
Results: A higher expression of LC3b II and a reduced expression of p62 observed in the Ang II-treated endothelial cells, as well as in the aorta of the hypertensive rats, indicated enhanced autophagy. Treatment with CHQ resulted in reduced autophagy flux (in vitro as well as in vivo) and suppressed Ang II-induced endothelial cell migration and angiogenesis (in vitro). The treatment with CHQ was also observed to prevent increase in blood pressure in hypertensive rats and preserved acetylcholine-induced relaxation in phenylephrine-contracted aorta from the hypertensive rats. In addition, chloroquine attenuated Ang II-induced contractions in the aorta of normotensive as well as hypertensive rats.
Conclusion: These observations indicated that CHQ lowers the blood pressure and preserves the vascular endothelial function during hypertension.

 

Keywords: Angiotensin II, Autophagy, Chloroquine, Endothelial function, Hypertension, Vascular dysfunction

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

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