Inhibition of galectin-3 ameliorates high-glucose-induced oxidative stress and inflammation in ARPE-19 cells

Li, Min; Tian, Meimei; Jiang, Xinli; Liu, Yan; Wang, Yan; Li, Yukun

doi:10.1080/15569527.2022.2081701

Cited by 10 publications

(4 citation statements)

References 48 publications

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“…Both cytosolic and mitochondrial ROS levels were markedly increased in ARPE-19 cells, confirming that the hyperglycemic state was characterized by high oxidative stress. Similar to previous studies, the present results showed that culturing ARPE-19 cells with HG leads to apoptosis and DNA damage via ROS generation [48][49][50][51]. However, in the presence of β-asarone, the production of ROS and induction of apoptosis and DNA damage were significantly abolished in HG-treated ARPE-19 cells.…”

Section: Discussionsupporting

confidence: 90%

β-Asarone Alleviates High-Glucose-Induced Oxidative Damage via Inhibition of ROS Generation and Inactivation of the NF-κB/NLRP3 Inflammasome Pathway in Human Retinal Pigment Epithelial Cells

et al. 2023

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Diabetic retinopathy (DR) is the leading cause of vision loss and a major complication of diabetes. Hyperglycemia-induced accumulation of reactive oxygen species (ROS) is an important risk factor for DR. β-asarone, a major component of volatile oil extracted from Acori graminei Rhizoma, exerts antioxidant effects; however, its efficacy in DR remains unknown. In this study, we investigated whether β-asarone inhibits high-glucose (HG)-induced oxidative damage in human retinal pigment epithelial (RPE) ARPE-19 cells. We found that β-asarone significantly alleviated cytotoxicity, apoptosis, and DNA damage in HG-treated ARPE-19 cells via scavenging of ROS generation. β-Asarone also significantly attenuated the excessive accumulation of lactate dehydrogenase and mitochondrial ROS by increasing the manganese superoxide dismutase and glutathione activities. HG conditions markedly increased the release of interleukin (IL)-1β and IL-18 and upregulated their protein expression and activation of the nuclear factor-kappa B (NF-κB) signaling pathway, whereas β-asarone reversed these effects. Moreover, expression levels of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome multiprotein complex molecules, including thioredoxin-interacting protein, NLRP3, apoptosis-associated speck-like protein containing a caspase-recruitment domain, and cysteinyl aspartate-specific proteinase-1, were increased in ARPE-19 cells under HG conditions. However, their expression levels remained similar to those in the control group in the presence of β-asarone. Therefore, β-asarone protects RPE cells from HG-induced injury by blocking ROS generation and NF-κB/NLRP3 inflammasome activation, indicating its potential as a therapeutic agent for DR treatment.

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Section: Discussionsupporting

confidence: 90%

β-Asarone Alleviates High-Glucose-Induced Oxidative Damage via Inhibition of ROS Generation and Inactivation of the NF-κB/NLRP3 Inflammasome Pathway in Human Retinal Pigment Epithelial Cells

et al. 2023

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“…TD139, a specific galectin-3 inhibitor, significantly reduces galectin-3 expression and oxidative stress of HMC3 cells [ 34 ]. Furthermore, galectin-3 knockdown reduces oxidative stress and apoptosis in ARPE-19 cells (spontaneously arising retinal pigment epithelial cell line) [ 37 ]. It is known that oxidative stress and apoptosis are pathophysiological features of cardiac dysfunction [ 38 ].…”

Section: Galectin-3 and Cardiac Inflammationmentioning

confidence: 99%

Role of Galectin in Cardiovascular Conditions including Cirrhotic Cardiomyopathy

2023

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Abnormal cardiac function in the setting of cirrhosis and in the absence of a primary cardiac disease is known as cirrhotic cardiomyopathy. The pathogenesis of cirrhotic cardiomyopathy is multifactorial but broadly is comprised of two pathways. The first is due to cirrhosis and synthetic liver failure with abnormal structure and function of many substances, including proteins, lipids, hormones, and carbohydrates such as lectins. The second is due to portal hypertension which invariably accompanies cirrhosis. Portal hypertension leads to a leaky, congested gut with resultant endotoxemia and systemic inflammation. This inflammatory phenotype comprises oxidative stress, cellular apoptosis, and inflammatory cell infiltration. Galectins exert all these pro-inflammatory mechanisms across many different tissues and organs, including the heart. Effective therapies for improving cardiac function in patients with cirrhosis are not available. Conventional strategies for other noncirrhotic heart diseases, including vasodilators, are not feasible because of the significant baseline vasodilation in cirrhotic patients. Therefore, exploring new treatment modalities for cirrhotic cardiomyopathy is of great importance. Galectin-3 inhibitors such as modified citrus pectin, N-acetyllactosamine, TD139 and GB0139 exert anti-apoptotic, anti-oxidative and anti-inflammatory effects and thus have potential therapeutic interest. This review briefly summarizes the physiological and pathophysiological role of galectin and specifically examines its role in cardiac disease processes. We present a more detailed discussion of galectin in cardiovascular complications of cirrhosis, particularly cirrhotic cardiomyopathy. Finally, therapeutic studies of galectin-3 inhibitors in cirrhotic cardiomyopathy are reviewed.

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“…Gal-3 is a carbohydrate-binding protein that plays important regulatory roles in inflammation, oxidative stress, apoptosis, and angiogenesis [19]. Evidence indicates that elevated Gal-3 expression participates in retinal tissue inflammation in diabetic animals [6] and RPE cell oxidative damage caused by high glucose [4].…”

Section: Original Papermentioning

confidence: 99%

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mentioning

confidence: 99%

Association of plasma galectin-3 and fetuin-A levels with diabetic retinopathy in type 2 diabetes mellitus patients

Li,

Tian,

Wang

et al. 2023

Endokrynol Pol

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lial cells, and sensory neurons [4]. Evidence indicates that Gal-3 overexpression in retina tissue [5, 6] and RPE cells [4] participates in the pathogenesis of DR. Gal-3 can be detected in circulation, and its level was found to be positively correlated with obesity, insulin resistance, DM, diabetic macrovascular complications, and diabetic nephropathy [7][8][9][10][11]. However, data about circulating Gal-3 levels and DR are limited.Fetuin-A (Fet-A) is a 64-kDa heterodimeric glycoprotein produced by the adipose tissue and liver [12]. Evidence indicates that circulating Fet-A is positively associated with insulin resistance, obesity, and T2DM [3]. Moreover, Fet-A was also found to stimulate pro-angiogenic factors, such as vascular endothelial growth factor (VEGF) [13][14][15]. Thus, the Fet-A level could be an early initiator of DR [13]. However, the cor-

show abstract

Inhibition of galectin-3 ameliorates high-glucose-induced oxidative stress and inflammation in ARPE-19 cells

Cited by 10 publications

References 48 publications

β-Asarone Alleviates High-Glucose-Induced Oxidative Damage via Inhibition of ROS Generation and Inactivation of the NF-κB/NLRP3 Inflammasome Pathway in Human Retinal Pigment Epithelial Cells

β-Asarone Alleviates High-Glucose-Induced Oxidative Damage via Inhibition of ROS Generation and Inactivation of the NF-κB/NLRP3 Inflammasome Pathway in Human Retinal Pigment Epithelial Cells

Role of Galectin in Cardiovascular Conditions including Cirrhotic Cardiomyopathy

Association of plasma galectin-3 and fetuin-A levels with diabetic retinopathy in type 2 diabetes mellitus patients

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