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Gene & Protein in Disease Dunaliella salina & myocardial ischemia-reperfusion injury
cardiomyopathy to human health has grown . The first injury through NRF2/KEAP1/antioxidant response
[1]
principle of treatment is to restore blood supply to the element (ARE) pathway activation . At the same time,
[14]
ischemic myocardium as soon as possible . However, the inflammatory damage during MIRI should not be
[2]
reperfusion might further aggravate myocardial injury. underestimated. The Janus kinase 2/signal transducer
This is known as myocardial ischemia-reperfusion injury and activator of transcription 3 (JAK2/STAT3) pathway
(MIRI) . A number of mechanisms are involved in it, is involved in various cardiovascular complications,
[3]
causing serious new dysfunction, including excessive including cardiomyocyte apoptosis, endoplasmic reticulum
[15]
inflammatory response, calcium ion (Ca ) overload, stress, oxidative stress, and inflammation . The rapid
2+
endoplasmic reticulum, and mitochondrial damage [4,5] . activation of JAK2/STAT3 pathway after I/R enhances
MIRI leads to an inflammatory response, resulting the transcription of inflammatory cytokines, which are
in inflammatory cell infiltration and accumulation of closely related to myocardial damage [5,16] . The inhibition of
proinflammatory factors . In addition, excessive oxidative JAK2/STAT3 pathway could reduce inflammatory damage
[5]
[17]
stress has also been reported to play an important role in rats suffering from MIRI . The present study aimed at
in MIRI. Previous research has identified the oxidative investigating the effect of D. salina on MIRI and the status
stress theory as one of the main etiologies of MIRI, which of KEAP1/NRF2 and JAK2/STAT3 signaling pathways
usually originates in either the excessive production of underlying D. salina against MIRI.
reactive oxygen species (ROS) or the decline of scavenging
capacity [6,7] . 2. Material and methods
Dunaliella salina, a halophilic green microalgae, rich 2.1. Experimental animals
in natural beta (β)-carotene, is considered an antioxidant C57BL/6J mice (male, 21–25 g) were obtained from
and anti-cancer compound, preventing night blindness, Laboratory Animal Center of Henan University of Science
delaying aging, and regulating immunity. In view of its and Technology (Luoyang, China; license number: SCXK
unique nutritional and functional components, D. salina 20190008). The mice were randomly divided into three
has the potential to be developed as a nutritional health food groups (n = 8 per group) after 1 week of adaptive feeding:
[8]
and authorized as additives for both humans and animals . (i) Control group; (ii) I/R group; and (3) I/R + D. salina
Hence, D. salina is considered a powerful antioxidant and group (500 mg/kg). All mice in the I/R + D. salina group
has excellent effect in preventing oxidative stress [9,10] . As were given D. salina by gavage for 7 days consecutively,
shown in mice, D. salina also has preventive effect on cornea whereas the other two groups of mice were given saline
injury induced by ultraviolet radiation, which may be due in the same way. All mice were kept in a controlled
to the increased activity of antioxidant defense system and environment (temperature, 22 ± 2°C; humidity, 50 ± 5%;
the inhibition of lipid peroxidation . A study has also 12 h light/dark cycle). The mice had unrestricted access to
[11]
shown that D. salina could exert therapeutic potential food and water.
against hepatic encephalopathy through its antioxidant, The study was approved by the Animal Care and Ethics
anti-inflammatory, and cytoprotective effects . Oral Committee of Henan University of Science and Technology
[12]
supplementation with D. salina has also shown to improve (Luoyang, China) and was performed in accordance with
cardiac dysfunction in obese rats . In addition, D. salina the National Institutes of Health Guidelines for the Care
[8]
has shown to ameliorate heart dysfunction associated with and Use of Laboratory Animals .
[18]
aging in rats induced by D-galactose . Whether or not
[10]
D. salina could alleviate MIRI, the involved mechanism 2.2. Langendorff perfused heart model
remains to be elucidated.
The mice were given intraperitoneal injection of ethyl
The kelch-like ECH-associated protein 1 (KEAP1)/ urethane (1 g/kg) for anesthesia and heparin (500 IU/kg)
nuclear factor (erythroid-derived 2)-like 2 (NRF2) signaling for heparinization. The hearts were removed from the
pathway is considered one of the most pivotal endogenous thoracic cavity and attached on the Langendorff apparatus.
antioxidative system . In brief, NRF2 and KEAP1 bind Perfusion was maintained at a constant pressure with
[13]
together in the cytoplasm physiologically. When stimulated, warmed (37.5°C) perfusate, and the hearts were immersed
NRF2 detaches from KEAP1, translocates to the nucleus, in a water-jacketed temperature-controlled glass chamber
and then promotes the expression of genes associated at 37.5°C, so as to ensure normothermia throughout the
with antioxidant activities, such as heme oxygenase-1 perfusion protocol. A latex balloon connected to the sensor
(HO-1) and quinone oxidoreductase 1 (NQO1) . Recent was inserted into the left ventricle of each heart through
[6]
studies have shown that suppressing oxidative stress left atrium incision. In the meantime, the heart rate, left
response could ameliorate ischemia/reperfusion (I/R) ventricular systolic pressure (LVSP), and electrocardiograph
Volume 2 Issue 2 (2023) 2 https://doi.org/10.36922/gpd.387

