Aloin Inhibits Müller Cells Swelling in a Rat Model of Thioacetamide-Induced Hepatic Retinopathy

Jung, Eun-Soo; Kim, Jung-Hyun

doi:10.3390/molecules23112806

Cited by 26 publications

(20 citation statements)

References 46 publications

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“…GFAP is upregulated during the light stress and blue light exposure, which leads to a nonspecific reactive change of Müller cells known as gliosis [ 55 , 56 ]. However, GFAP accumulation in Müller cells was reported as an essential photoreceptor stress parameter in retinopathy induced rats, in accordance with our findings [ 57 ]. In a recent study, a pattern of GFAP ADPase staining also suggested a robust Müller cells/astrocytes reactivity in the Goto-Kakizaki rat retina [ 58 ].…”

Section: Discussionsupporting

confidence: 93%

Different Doses of β‐Cryptoxanthin May Secure the Retina from Photooxidative Injury Resulted from Common LED Sources

Orhan

Tuzcu

Gençoğlu

et al. 2021

Oxidative Medicine and Cellular Longevity

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Retinal damage associated with loss of photoreceptors is a hallmark of eye diseases such as age-related macular degeneration (AMD) and diabetic retinopathy. Potent nutritional antioxidants were previously shown to abate the degenerative process in AMD. β-Cryptoxanthin (BCX) is an essential dietary carotenoid with antioxidant, anti-inflammatory, and provitamin A activity. It is a potential candidate for developing intervention strategies to delay the development/progression of AMD. In the current study, the effect of a novel, highly purified BCX oral formulation on the rat retinal damage model was evaluated. Rats were fed with BCX for four weeks at the doses of 2 and 4 mg/kg body weight in the form of highly bioavailable oil suspension, followed by retinal damage by exposing to the bright light-emitting diode (LED) light (750 lux) for 48 hrs. Animals were sacrificed after 48 hours, and eyes and blood samples were collected and analyzed. BCX supplementations (2 and 4 mg/kg) showed improvements in the visual condition as demonstrated by histopathology of the retina and measured parameters such as total retinal thickness and outer nuclear layer thickness. BCX supplementation helped reduce the burden of oxidative stress as seen by decreased serum and retinal tissue levels of malondialdehyde (MDA) and restored the antioxidant enzyme activities in BCX groups. Further, BCX supplementation modulated inflammatory markers (IL-1β, IL-6, and NF-κB), apoptotic proteins (Bax, Bcl-2, caspase 3), growth proteins and factors (GAP43, VEGF), glial and neuronal proteins (GFAP, NCAM), and heme oxygenase-1 (HO-1), along with the mitochondrial stress markers (ATF4, ATF6, Grp78, Grp94) in the rat retinal tissue. This study indicates that oral supplementation of BCX exerts a protective effect on light-induced retinal damage in the rats via reducing oxidative stress and inflammation, also protected against mitochondrial DNA damage and cellular death.

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Section: Discussionsupporting

confidence: 93%

Different Doses of β‐Cryptoxanthin May Secure the Retina from Photooxidative Injury Resulted from Common LED Sources

Orhan

Tuzcu

Gençoğlu

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…AL is one of the main active components in the leaf exudates of the Aloe vera plant, accounting for about 15%–40% [25]. An extensive literature review indicates that AL significantly increases the liver enzymes and improves the pathological changes in liver tissues in the models of chronic alcoholic liver injury [26] and thioacetamide- (TAA-) induced hepatic retinopathy [27]. Moreover, the protective effect of AL was documented before in I/R injury that occurred in the PC12 cells [28] and the heart [10, 29].…”

Section: Discussionmentioning

confidence: 99%

Aloin Preconditioning Attenuates Hepatic Ischemia/Reperfusion Injury via Inhibiting TLR4/MyD88/NF-κB Signal PathwayIn VivoandIn Vitro

Qian

Gao

et al. 2019

Oxidative Medicine and Cellular Longevity

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Background Aloin exerts considerable protective effects in various disease models, and its effect on hepatic ischemia-reperfusion (HIR) injury remains unknown. This research is aimed at conducting an in-depth investigation of the antioxidant, anti-inflammatory, and antiapoptosis effects of aloin in HIR injury and explain the underlying molecular mechanisms. Methods In vivo, different concentrations of aloin were intraperitoneally injected 1 h before the establishment of the HIR model in male mice. The hepatic function, pathological status, oxidative stress, and inflammatory and apoptosis markers were measured. In vitro, aloin (AL, C21H22O9) or lipopolysaccharide (LPS) was added to a culture of mouse primary hepatocytes before it underwent hypoxia/reoxygenation (H/R), and the apoptosis in the mouse primary hepatocytes was analyzed. Results We found that 20 mg/kg was the optimum concentration of aloin for mitigating I/R-induced liver tissue damage, characterized by decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Aloin pretreatment substantially suppressed the generation of hepatic malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), and IL-6 and enhanced the hepatic superoxide dismutase (SOD) activities as well as glutathione (GSH) and IL-10 levels in the liver tissue of I/R mice; this indicated that aloin ameliorated I/R-induced liver damage by reducing the oxidative stress and inflammatory response. Moreover, aloin inhibited hepatocyte apoptosis and inflammatory response that was caused by the upregulated expression of Bcl-2, the downregulated expression of cleaved caspase3(C-caspase3), Bax, Toll-like receptor 4 (TLR4), FADD, MyD88, TRAF6, phosphorylated IKKα/β (p-IKKα/β), and phosphorylated nuclear factor κB p65 (p-NF-κB p65).

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“…Sun et al ( 91 ) observed in rat model of DR that after the application of the potassium channel opener pinadil, the expression of Kir4.1 was upregulated, the function of Müller cells was improved and the symptoms of retinal macular edema were alleviated. Another study suggested that aloe vera may help protect from retinal damage associated with liver failure by normalizing Kir4.1 and AQP4 through reducing oxidative stress and inflammation ( 92 ).…”

Section: Prospectsmentioning

confidence: 99%

Kir4.1 may represent a novel therapeutic target for diabetic retinopathy (Review)

et al. 2021

Exp Ther Med

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As the major cause of irreversible loss of vision in adults, diabetic retinopathy (DR) is one of the most serious complications of diabetes. The imbalance of the retinal microenvironment and destruction of the blood-retinal barrier have a significant role in the progression of DR. Inward rectifying potassium channel 4.1 (Kir4.1) is located on Müller cells and is closely related to potassium homeostasis, water balance and glutamate clearance in the whole retina. The present review discusses the functions of Kir4.1 in regulating the retinal microenvironment and related biological mechanisms in DR. In the future, Kir4.1 may represent a novel alternative therapeutic target for DR through affecting the retinal microenvironment.

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Aloin Inhibits Müller Cells Swelling in a Rat Model of Thioacetamide-Induced Hepatic Retinopathy

Cited by 26 publications

References 46 publications

Different Doses of β‐Cryptoxanthin May Secure the Retina from Photooxidative Injury Resulted from Common LED Sources

Different Doses of β‐Cryptoxanthin May Secure the Retina from Photooxidative Injury Resulted from Common LED Sources

Aloin Preconditioning Attenuates Hepatic Ischemia/Reperfusion Injury via Inhibiting TLR4/MyD88/NF-κB Signal PathwayIn VivoandIn Vitro

Kir4.1 may represent a novel therapeutic target for diabetic retinopathy (Review)

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