Azithromycin inhibited oxidative stress and apoptosis of high glucose‐induced podocytes by inhibiting <scp>STAT1</scp> pathway

Xing, Yu; Liu, Kuan Zhi

doi:10.1002/ddr.21801

Cited by 6 publications

(4 citation statements)

References 25 publications

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“…However, when oxidative stress overpowers the redox balance, it leads to the proinflammatory environment, which plays an important role in neurovascular degeneration in retinal diseases. ,, Because of their defensive function, microglia have a very strong antioxidant system. Still, the oxidative stress becomes detrimental and leads to cell death in microglia. ,,, Interestingly, AZM could prevent the intracellular oxidative stress formation in glia which is corroborative with earlier findings, in which AZM exhibited antioxidant activity in the high glucose-induced podocyte . These antioxidant properties of AZM could be ensued by nuclear translocation of Nrf2 and hence increasing the expression of downstream antioxidant genes. , By virtue of the inhibition of oxidative stress, the AZM pretreatment could prevent the microglia from entering into the proinflammatory phase and inhibits the secretion of inflammatory cytokines such as IL-1β and TNF-α.…”

Section: Discussionsupporting

confidence: 83%

“… 15 , 17 , 40 , 41 Interestingly, AZM could prevent the intracellular oxidative stress formation in glia which is corroborative with earlier findings, in which AZM exhibited antioxidant activity in the high glucose-induced podocyte. 42 These antioxidant properties of AZM could be ensued by nuclear translocation of Nrf2 and hence increasing the expression of downstream antioxidant genes. 43 , 44 By virtue of the inhibition of oxidative stress, the AZM pretreatment could prevent the microglia from entering into the proinflammatory phase and inhibits the secretion of inflammatory cytokines such as IL-1β and TNF-α.…”

Section: Discussionmentioning

confidence: 99%

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Azithromycin Protects Retinal Glia Against Oxidative Stress-Induced Morphological Changes, Inflammation, and Cell Death

Mahaling

Pandala

Wang

et al. 2022

ACS Bio Med Chem Au

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The reactivity of retinal glia in response to oxidative stress has a significant effect on retinal pathobiology. The reactive glia change their morphology and secret cytokines and neurotoxic factors in response to oxidative stress associated with retinal neurovascular degeneration. Therefore, pharmacological intervention to protect glial health against oxidative stress is crucial for maintaining homeostasis and the normal function of the retina. In this study, we explored the effect of azithromycin, a macrolide antibiotic with antioxidant, immunomodulatory, anti-inflammatory, and neuroprotective properties against oxidative stress-induced morphological changes, inflammation, and cell death in retinal microglia and Müller glia. Oxidative stress was induced by H2O2, and the intracellular oxidative stress was measured by DCFDA and DHE staining. The change in morphological characteristics such as the surface area, perimeter, and circularity was calculated using ImageJ software. Inflammation was measured by enzyme-linked immunosorbent assays for TNF-α, IL-1β, and IL-6. Reactive gliosis was characterized by anti-GFAP immunostaining. Cell death was measured by MTT assay, acridine orange/propidium iodide, and trypan blue staining. Pretreatment of azithromycin inhibits H2O2-induced oxidative stress in microglial (BV-2) and Müller glial (MIO-M1) cells. We observed that azithromycin inhibits oxidative stress-induced morphological changes, including the cell surface area, circularity, and perimeter in BV-2 and MIO-M1 cells. It also inhibits inflammation and cell death in both the glial cells. Azithromycin could be used as a pharmacological intervention on maintaining retinal glial health during oxidative stress.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Azithromycin Protects Retinal Glia Against Oxidative Stress-Induced Morphological Changes, Inflammation, and Cell Death

Mahaling

Pandala

Wang

et al. 2022

ACS Bio Med Chem Au

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“…We would like to confirm that some non-specific FDA-approved drugs augment our natural interferon response while inhibiting and disrupting NF-κB signaling, including our repurposed Kelleni's immunomodulatory COVID-19 protocol that was shown to restore homeostasis of the SARS-CoV-2 inhibited and/or dysregulated interferon response (Kelleni, 2020b(Kelleni, , 2021a as well as to inhibit the concomitant SARS-CoV-2-induced robust activation of the IL-6 amplifier including NF-κB signaling as an essential component (Smart et al 2020;Kelleni 2021b) which was also showed by Nilsson-Payant and colleagues to play a fundamental role in SARS-CoV-2 replication (Nilsson-Payant Benjamin et al 2021). Moreover, we suggest that azithromycin might also disrupt the NF-κB and signal transducer and activator of transcription-1 synergistic induction of inflammatory genes expression that could also play a role in the dysregulated COVID-19 immune response (Hiroi and Ohmori 2005;Xing and Liu 2021).…”

Section: Kelleni's Protocol Might Inhibit Sars-cov-2 Replicationmentioning

confidence: 93%

NSAIDs and Kelleni’s protocol as potential early COVID-19 treatment game changer: could it be the final countdown?

Kelleni

2021

Inflammopharmacol

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We have previously published several papers illustrating numerous immunomodulatory and anti-inflammatory potential benefits when we repurposed safe, generic non-steroidal anti-inflammatory drugs (NSAIDs)/nitazoxanide/azithromycin (Kelleni's protocol), to early manage our COVID-19 pediatric, adult, and pregnant patients. In this manuscript, we discuss some recently published meta-analysis and clinical studies supporting our practice and discuss a molecular study that might be interpreted as an academic proof that our protocol might also prevent SARS-CoV-2 replication. Moreover, after aspirin has been suggested to be independently associated with reduced risk of mechanical ventilation, ICU admission and inhospital mortality of COVID-19, we claim that the molecular interpretation of the results that led to this suggestion was not scientifically accurate, and we provide our academic interpretation confirming that low-dose aspirin is least likely to improve COVID-19 mortality through anticoagulation as was suggested. Furthermore, we describe other potential benefits related to aspirin-triggered lipoxins and resolvins while illustrating how NSAIDs interfere with COX-1, COX-2, SARS-CoV-2/ SARS-CoV-2 ORF protein-dependent activation of caspases and their subsequent mitochondrial dysfunction, endoplasmic reticulum stress, apoptosis and necroptosis which were associated with COVID-19 complications. Similarly, NSAIDs are known caspase inhibitors and thus they might independently inhibit other caspase-related COVID-19-associated downstream pathological signaling mechanisms. Finally, we postulated that CARD-14, a caspase recruitment domain-containing protein, polymorphisms might play a role in the development of severe and critical COVID-19 and confirmed our old call to early adopt NSAIDs, as an integral part of Kelleni's protocol, as of choice in its management aiming to end this pandemic.

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“…Consequently, it may be of therapeutic benefit in various inflammatory disorders and to prevent graft-versus-host disease in patients undergoing stem-cell transplantation [167][168][169]. Furthermore, azithromycin has a therapeutic effect on diabetes as it inhibits oxidative stress, inflammation and apoptosis [170]. It combats epithelial barrier dysfunctions [171,172] and promotes connective tissue remodeling [173].…”

Section: Use Of Immunomodulatory Antibioticsmentioning

confidence: 99%

Bone Formation and Maintenance in Oral Surgery: The Decisive Role of the Immune System—A Narrative Review of Mechanisms and Solutions

Choukroun,

Parnot,

Surmenian

et al. 2024

Bioengineering

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Based on the evidence of a significant communication and connection pathway between the bone and immune systems, a new science has emerged: osteoimmunology. Indeed, the immune system has a considerable impact on bone health and diseases, as well as on bone formation during grafts and its stability over time. Chronic inflammation induces the excessive production of oxidants. An imbalance between the levels of oxidants and antioxidants is called oxidative stress. This physio-pathological state causes both molecular and cellular damage, which leads to DNA alterations, genetic mutations and cell apoptosis, and thus, impaired immunity followed by delayed or compromised wound healing. Oxidative stress levels experienced by the body affect bone regeneration and maintenance around teeth and dental implants. As the immune system and bone remodeling are interconnected, bone loss is a consequence of immune dysregulation. Therefore, oral tissue deficiencies such as periodontitis and peri-implantitis should be regarded as immune diseases. Bone management strategies should include both biological and surgical solutions. These protocols tend to improve immunity through antioxidant production to enhance bone formation and prevent bone loss. This narrative review aims to highlight the relationship between inflammation, oxidation, immunity and bone health in the oral cavity. It intends to help clinicians to detect high-risk situations in oral surgery and to propose biological and clinical solutions that will enhance patients’ immune responses and surgical treatment outcomes.

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Azithromycin inhibited oxidative stress and apoptosis of high glucose‐induced podocytes by inhibiting STAT1 pathway

Cited by 6 publications

References 25 publications

Azithromycin Protects Retinal Glia Against Oxidative Stress-Induced Morphological Changes, Inflammation, and Cell Death

Azithromycin Protects Retinal Glia Against Oxidative Stress-Induced Morphological Changes, Inflammation, and Cell Death

NSAIDs and Kelleni’s protocol as potential early COVID-19 treatment game changer: could it be the final countdown?

Bone Formation and Maintenance in Oral Surgery: The Decisive Role of the Immune System—A Narrative Review of Mechanisms and Solutions

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