Neuroprotective Effect of Intravitreal Single-Dose Lithium Chloride after Optic Nerve Injury in Rats

Ala, Moein; Jafari, Razieh Mohammad; Nematian, Hossein; Ganjedanesh, Mohammad Reza; Naderi, Asieh; Akbariani, Mostafa; Sanatkar, Mehdi; Satarian, Leila; Fard, Masoud Aghsaei; Dehpour, Ahmad Reza

doi:10.1080/02713683.2020.1808999

Cited by 10 publications

(5 citation statements)

References 31 publications

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“…In an optic nerve injury model in rats, the neuroprotective effects of LiCl can be attributed to various mechanisms, such as upregulation of antiapoptotic proteins, suppression of proinflammatory molecules and proapoptotic factors, and decreased nitric oxide. 28 Several mediators, including N -methyl- d -aspartate receptors, the PI3K/Akt pathway, cytoprotective Bcl-2, and glycogen synthase kinase-3 beta (GSK-3β), are implicated in the process underlying LiCl-induced neuroprotection, which could promote RGC survival and axon regeneration. 29 – 31 In the present study, our results also indicated that LiCl dramatically decreased the expression of cleaved caspase 3 and increased the Bcl-2/BAX ratio, thus inhibiting microglial-induced apoptosis of the retinal neurocytes.…”

Section: Discussionmentioning

confidence: 99%

Lithium Chloride Exerts Anti-Inflammatory and Neuroprotective Effects by Inhibiting Microglial Activation in LPS-Induced Retinal Injury

Luo

Huang

et al. 2023

Invest. Ophthalmol. Vis. Sci.

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Purpose To explore the anti-inflammatory and neuroprotective effects of lithium chloride (LiCl) in LPS-induced retinal injury. Methods In vitro, primary retinal microglia were pretreated with LiCl and stimulated with lipopolysaccharide (LPS). Pro-inflammatory cytokine production, microglial morphological changes, and inflammation-associated signaling pathways were measured by real-time PCR (RT-PCR), western blotting, and immunofluorescence. Primary retinal neurons were cultured with microglial-derived conditioned medium in the absence or presence of LiCl. Neurotoxicity was evaluated by Cell Counting Kit-8 (CCK-8), terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, and γ-H2AX detection. In vivo, an endotoxin-induced uveitis mice model was established, and each animal was given intraperitoneal injection of LiCl or vehicle. The retinal inflammatory response was measured by hematoxylin and eosin and fluorescent staining, RT-PCR, western blotting, and TUNEL assay. Retinal thickness and function were evaluated by spectral-domain optical coherence tomography and electroretinography. Results In vitro, LiCl exerted no obvious toxic effects on microglia and significantly decreased proinflammatory factor (inducible nitric oxide synthase, tumor necrosis factor α, interleukin 6) production, inhibited microglial activation in morphology, and suppressed nuclear factor kappa B (NF-κB), Akt, and phosphatidylinositol 3-kinase (PI3K) phosphorylation. Moreover, LiCl promoted retinal neuron survival and reduced cell apoptosis and the expression of γ-H2AX. In vivo, LiCl reduced inflammatory infiltrating cells in the vitreous cavity and decreased proinflammatory cytokine expression in retinas. LiCl suppressed LPS-induced microglial activation, proliferation, and migration. Additionally, LiCl reduced LPS-induced apoptosis of ganglion cells and retinal edema and rescued retinal functional damage. Conclusions This study demonstrates that LiCl exerts anti-inflammatory and neuroprotective effects by inhibiting microglial activation via the PI3K/Akt/NF-κB pathway in LPS-induced retinal injury. LiCl provides a novel and promising option to treat retinal inflammatory diseases.

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Section: Discussionmentioning

confidence: 99%

Lithium Chloride Exerts Anti-Inflammatory and Neuroprotective Effects by Inhibiting Microglial Activation in LPS-Induced Retinal Injury

Luo

Huang

et al. 2023

Invest. Ophthalmol. Vis. Sci.

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“…At the end of the experiment, all rats were anesthetized with a cocktail of i.p. ketamine/xylazine (87/13 mg/kg) injected at the dose of 1 mL/kg ( Ala et al, 2021 ), then blood samples were collected from retro-orbital sinus and left to clot for 1 h at room temperature, then centrifuged at 3,000 rpm for 15 min to separate sera. Subsequently, all rats were sacrificed by decapitation and the heart was dissected and divided into two portions.…”

Section: Methodsmentioning

confidence: 99%

The cardioprotective effects of secoisolariciresinol diglucoside (flaxseed lignan) against cafeteria diet-induced cardiac fibrosis and vascular injury in rats: an insight into apelin/AMPK/FOXO3a signaling pathways

et al. 2023

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Introduction: Fast food is a major risk factor for atherosclerosis, a leading cause of morbidity and mortality in the Western world. Apelin, the endogenous adipokine, can protect against cardiovascular disease via activating its receptor, APJ. Concurrently, secoisolariciresinol diglucoside (SDG), a flaxseed lignan extract (FLE), showed a therapeutic impact on atherosclerosis. The current study aimed to examine the effect of SDG on cafeteria diet (CAFD)-induced vascular injury and cardiac fibrosis via tracking the involvement of the apelin/APJ pathway.Methods: Thirty male rats were allocated into control, FLE-, CAFD-, CAFD/FLE-, and CAFD/FLE/F13A-treated rats, where F13A is an APJ blocker. All treatments lasted for 12 weeks.Results and discussion: The CAFD-induced cardiovascular injury was evidenced by histological distortions, dyslipidemia, elevated atherogenic indices, cardiac troponin I, collagen percentage, glycogen content, and apoptotic markers. CAFD increased both the gene and protein expression levels of cardiac APJ, apelin, and FOXO3a, in addition to increasing endothelin-1, VCAM1, and plasminogen activator inhibitor-1 serum levels and upregulating cardiac MMP-9 gene expression. Moreover, CAFD reduced serum paraoxonase 1 and nitric oxide levels, cardiac AMPK, and nuclear Nrf2 expression. FLE attenuated CAFD-induced cardiovascular injury. Such effect was reduced in rats receiving the APJ blocker, implicating the involvement of apelin/APJ in FLE protective mechanisms.Conclusion: FLE supplementation abrogated CAFD-induced cardiac injury and endothelial dysfunction in an apelin/APJ-dependent manner.

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“…The procedure of western blotting analysis was conducted as previously published (Ala et al, 2021; Lu et al, 2020). Dissected hippocampal tissues ( n = 3 for each group) were homogenized in the radioimmunoprecipitation assay lysis buffer with protease and phosphatase inhibitor cocktail (Sigma Aldrich, St. Louis, MO).…”

Section: Methodsmentioning

confidence: 99%

Soy isoflavones protects against cognitive deficits induced by chronic sleep deprivation via alleviating oxidative stress and suppressing neuroinflammation

Lü

Wei

Jiang

et al. 2022

Phytotherapy Research

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Mounting evidence suggests that there is a close association between chronic sleep deprivation (CSD) and cognitive deficits. The animal model of CSD‐induced cognitive deficits is commonly used to seek potential treatments. Soy isoflavones (SI) have been reported to possess antioxidant, anti‐inflammation, and neuroprotective effects. In the present study, the effects of SI on CSD‐induced memory impairment were investigated. The mice were subjected to the sleep interruption apparatus and continuously sleep deprived for 2 weeks, while orally administrated with SI (10, 20, and 40 mg/kg) or Modafinil (MOD,100 mg/kg) during the CSD process. Immediately after the SD protocol, cognitive performance of mice was evaluated by the object location recognition (OLR) test, the novel object recognition (NOR) test, and the Morris water maze (MWM) task, as well as the hippocampus, was extracted for evaluation of oxidative stress parameters and inflammation levels through biochemical parameter assay and western blotting analysis. The results showed that SI administration remarkably improved the cognitive performance of CSD‐treated mice in OLR, NOR, and MWM tests. In addition, SI significantly elevated total antioxidant capacity and superoxide dismutase enzyme activities, decreased malondialdehyde level, promoting antioxidant element nuclear erythroid‐2‐related factor 2, and its downstream targets, including heme oxygenase 1, and quinone oxidoreductase 1 protein expressions. Moreover, SI treatment significantly suppressed nuclear factor kappa B p65, nitric oxide synthase, and cyclooxygenase 2 activation, as well as the pro‐inflammatory cytokines (Tumor necrosis factor‐α [TNF‐α], interleukin‐6 [IL‐6], and interleukin‐1β [IL‐1β]) release in the hippocampus of CSD‐treated mice. In summary, the current study provides an insight into the potential of SI in treatment of cognitive deficits by CSD.

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Neuroprotective Effect of Intravitreal Single-Dose Lithium Chloride after Optic Nerve Injury in Rats

Cited by 10 publications

References 31 publications

Lithium Chloride Exerts Anti-Inflammatory and Neuroprotective Effects by Inhibiting Microglial Activation in LPS-Induced Retinal Injury

Lithium Chloride Exerts Anti-Inflammatory and Neuroprotective Effects by Inhibiting Microglial Activation in LPS-Induced Retinal Injury

The cardioprotective effects of secoisolariciresinol diglucoside (flaxseed lignan) against cafeteria diet-induced cardiac fibrosis and vascular injury in rats: an insight into apelin/AMPK/FOXO3a signaling pathways

Soy isoflavones protects against cognitive deficits induced by chronic sleep deprivation via alleviating oxidative stress and suppressing neuroinflammation

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