Magnolol limits NFκB-dependent inflammation by targeting PPARγ relieving retinal ischemia/reperfusion injury

Wang, Ning; Yang, Yijie; Liu, Yixin; Huang, Lulu; Gu, Mengyang; Wu, Yue; Xu, Li; Sun, Hao; Guo, Wu

doi:10.1016/j.intimp.2022.109242

Cited by 8 publications

(4 citation statements)

References 53 publications

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“…A significant increase was observed in TNF-α, IL-1β, and IL-6 levels in the eye tissues of rats in the I/R-mediated OIS model. These findings were consistent with those obtained in the studies conducted by Wang et al [32] . LTC prevented the increase of TNF-α, IL-1β, and IL-6 in I/R treated eye tissue more significantly than lacidipine and TPP treated alone.…”

Section: Ltc In Ocular Ischemic Syndromesupporting

confidence: 94%

Lacidipine, thiamine pyrophosphate and their combination on the ocular ischemic syndrome induced by bilateral common carotid artery ligation

Cicek,

Altuner,

Suleyman

et al. 2024

Int J Ophthalmol

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AIM: To investigate the effect of lacidipine, thiamine pyrophosphate (TPP) and the combination of lacidipine and TPP against oxidative and inflammatory eye damage induced by bilateral common carotid artery ligation in rats. METHODS: Male albino Wistar rats were categorized as those who underwent sham surgery (SG), right and left common carotid cross-clamping and unclamping procedure (CCU), lacidipine+CCU (LCCU), TPP+CCU (TCCU), and combination of lacidipine and TPP (LTC)+CCU (LTCCU). One hour before anesthesia, the LCCU (n=6) received lacidipine (4 mg/kg, orally) and the TCCU (n=6) received TPP (20 mg/kg, intraperitoneally). The SG (n=6) and CCU (n=6) received the same volume of distilled water from the same route. After anesthesia (60 mg/kg ketamine, intraperitoneally), the necks of the rats were opened in the midline. Ischemia was created for 10min by placing clips on the right and left common carotid arteries. Rats in the SG only underwent subcutaneous incision. After 10min, the clips were removed and reperfusion was achieved for six days. Then, the animals were euthanized (120 mg/kg ketamine, intraperitoneally) and the levels of oxidant, antioxidant and proinflammatory cytokines in the eye tissues were determined. The retinal tissue of the eye was also examined histopathologically. RESULTS: Lacidipine, TPP, and LTC significantly prevent the increase in malondialdehyde, tumor necrosis factor-alpha, interleukin-1β (IL-1β), and IL-6 levels, decrease in total glutathione levels, superoxide dismutase and catalase activities and histopathological retinal damage in eye tissue induced by bilateral common carotid artery ligation in rats. The impact of these drugs on protection is determined to be LTC>lacidipine>TPP. CONCLUSION: As a result of the study, it is concluded that LTC may be more effective than lacidipine and TPP alone in treating ocular ischemic syndrome.

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Section: Ltc In Ocular Ischemic Syndromesupporting

confidence: 94%

Lacidipine, thiamine pyrophosphate and their combination on the ocular ischemic syndrome induced by bilateral common carotid artery ligation

Cicek,

Altuner,

Suleyman

et al. 2024

Int J Ophthalmol

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“…Nevertheless, the present study is the first to demonstrate the implicit time-decreasing effect of BGP (Figures 4B,D and 8B). Similar anti-ischemic retinal protection of other agents was shown by various authors [43,47], although some even reported unchanged implicit times despite other evident effects on the electroretinogram [48].…”

Section: Discussionsupporting

confidence: 84%

“…A similar protective effect is a hallmark of other anti-ischemic agents as well [ 31 , 32 , 49 ]. It is well documented that a common consequence of ischemia–reperfusion injury is edema [ 46 , 50 ], and then necro-apopto-autophagy, i.e., initiation of different cell-death mechanisms, resulting in thinning of retinal layers [ 47 , 51 , 52 ]. Edema, however, may be transient, which implies a reversible injury as well [ 46 , 53 ].…”

Section: Discussionmentioning

confidence: 99%

Electroretinographical Analysis of the Effect of BGP-15 in Eyedrops for Compensating Global Ischemia–Reperfusion in the Eyes of Sprague Dawley Rats

Takács,

Szilágyi,

Priksz

et al. 2024

Biomedicines

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Retinal vascular diseases and consequential metabolic disturbances in the eye are major concerns for healthcare systems all around the world. BGP-15, a drug candidate small-molecule [O-(3-piperidino-2-hydroxy-1-propyl) nicotinic amidoxime dihydrochloride], has been formerly demonstrated by our workgroup to be retinoprotective both in the short and long term. Based on these results, the present study was performed to investigate the efficacy of BGP in an eyedrop formulation containing sulfobutylether-β-cyclodextrin (SBECD), which is a solubility enhancer as well. Electroretinographical evaluations were carried out and BGP was demonstrated to improve both scotopic and photopic retinal a- and b-waves, shorten their implicit times and restore oscillatory potentials after ischemia–reperfusion. It was also observed to counteract retinal thinning after ischemia–reperfusion in the eyes of Sprague Dawley rats. This small-molecule drug candidate is able to compensate for experimental global eye ischemia–reperfusion injury elicited by ligation of blood vessels in rats. We successfully demonstrated that BGP is able to exert its protective effects on the retina even if administered in the form of eyedrops.

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“…I t is generally accepted that ischaemia-reperfusion (I/R)induced tissue damage is not only related to the degree of reduced blood flow, but also to intracellular calcium overload, oxidative stress, inflammatory responses, neurotoxicity of excitatory amino acids, excessive nitric oxide synthesis, and disturbances in energy metabolism [1] , ultimately causing tissue damage and neuronal cell necrosis/apoptosis with the process causing an increase in reactive oxygen species (ROS), including superoxide (O 2-), hydrogen peroxide (H 2 O 2 ) and hydroxyl radicals, leading to DNA fracture, lipid peroxidation and protein inactivation [2][3] . The mechanisms by which I/R injury to tissue occurs are complex and include primary injury in the early stages of ischaemia and secondary injury following reperfusion [4] , which is further exacerbated by I/R caused by the restoration of tissue blood supply after ischaemia has occurred.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of ginsenoside Rg1 on 661W cells exposed to oxygen-glucose deprivation/reperfusion via keap1/nrf2 pathway

Zhou¹,

Xie²,

Zhou³

et al. 2023

Int J Ophthalmol

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AIM: To construct an in vitro model of oxygen-glucose deprivation/reperfusion (OGD/R) induced injury to the optic nerve and to study the oxidative damage mechanism of ischemia-reperfusion (I/R) injury in 661W cells and the protective effect of ginsenoside Rg1. METHODS: The 661W cells were treated with different concentrations of Na2S2O4 to establish OGD/R model in vitro. Apoptosis, intracellular reactive oxygen species (ROS) levels and superoxide dismutase (SOD) levels were measured at different time points during the reperfusion injury process. The injury model was pretreated with graded concentrations of ginsenoside Rg1. Real-time polymerase chain reaction (PCR) was used to measure the expression levels of cytochrome C (cyt C)/B-cell lymphoma-2 (Bcl2)/Bcl2 associated protein X (Bax), heme oxygenase-1 (HO-1), caspase9, nuclear factor erythroid 2-related factor 2 (nrf2), kelch-like ECH-associated protein 1 (keap1) and other genes. Western blot was used to detect the expression of nrf2, phosphorylated nrf2 (pnrf2) and keap1 protein levels. RESULTS: Compared to the untreated group, the cell activity of 661W cells treated with Na2S2O4 for 6 and 8h decreased (P<0.01). Additionally, the ROS content increased and SOD levels decreased significantly (P<0.01). In contrast, treatment with ginsenoside Rg1 reversed the cell viability and SOD levels in comparison to the Na2S2O4 treated group (P<0.01). Moreover, Rg1 reduced the levels of caspase3, caspase9, and cytC, while increasing the Bcl2/Bax level. These differences were all statistically significant (P<0.05). Western blot analysis showed no significant difference in the protein expression levels of keap1 and nrf2 with Rg1 treatment, however, Rg1 significantly increased the ratio of pnrf2/nrf2 protein expression compared to the Na2S2O4 treated group (P<0.001). CONCLUSION: The OGD/R process is induced in 661W cells using Na2S2O4. Rg1 inhibits OGD/R-induced oxidative damage and alleviates the extent of apoptosis in 661W cells through the keap1/nrf2 pathway. These results suggest a potential protective effect of Rg1 against retinal I/R injury.

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Magnolol limits NFκB-dependent inflammation by targeting PPARγ relieving retinal ischemia/reperfusion injury

Cited by 8 publications

References 53 publications

Lacidipine, thiamine pyrophosphate and their combination on the ocular ischemic syndrome induced by bilateral common carotid artery ligation

Lacidipine, thiamine pyrophosphate and their combination on the ocular ischemic syndrome induced by bilateral common carotid artery ligation

Electroretinographical Analysis of the Effect of BGP-15 in Eyedrops for Compensating Global Ischemia–Reperfusion in the Eyes of Sprague Dawley Rats

Protective effect of ginsenoside Rg1 on 661W cells exposed to oxygen-glucose deprivation/reperfusion via keap1/nrf2 pathway

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