Oxidative Stress and Inflammation, 2nd Volume

Topic Information

Dear Colleagues,

Oxidative stress is viewed as an imbalance between the production of reactive oxygen species (ROS) and their elimination by protective mechanisms, which can lead to chronic inflammation. The incorrect lifestyle and the intake of external unhealthy chemicals are the major causes of age-related chronic diseases and cancer. Their study includes diseases pathology pathway, lifestyle, treatment, protection, and prevention of oxidative stress and inflammation. ROS are normally produced within the body in limited amount and are essential compounds involved in the regulation of processes capable of maintaining cell homeostasis and functions (signal transduction, gene expression, and activation of receptors). This imbalance may cause oxidative stress, which can lead to lipid peroxidation, gene mutation, inflammation and other complications. The harmful oxidative activity of ROS can be counteracted only by antioxidant/anti-inflammatory compounds, which may be both synthetic and natural, but are often characterized by several stability issues, such as poor water solubility and low bioavailability, that compromise their in vivo activities. The research papers of this Topic are looked forward to providing an overview of the status of research on both natural and synthetic products with antioxidant properties and capable of counteracting inflammatory diseases, including, but not necessarily restricted to, chemical compounds synthetic or of natural origin, vitamins, peptides, micronutrients, non-starch polysaccharides, probiotics, postbiotics, prebiotics formulations containing functional foods or nutraceutical or cosmeceutical products and their innovative oral, systemic or topical delivery capable to overcome their stability issues.

Dr. Maria Letizia Manca
Dr. Amparo Nacher
Dr. Mohamad Allaw
Dr. Matteo Perra
Dr. Ines Castangia
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomedicines biomedicines	3.9	5.2	2013	14.6 Days	CHF 2600
Cells cells	5.1	9.9	2012	17 Days	CHF 2700
International Journal of Molecular Sciences ijms	4.9	8.1	2000	16.8 Days	CHF 2900
Life life	3.2	4.3	2011	17.8 Days	CHF 2600
Oxygen oxygen	-	-	2021	19 Days	CHF 1000

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Open AccessArticle

Low Iron Diet Improves Clinical Arthritis in the Mouse Model of Collagen-Induced Arthritis

by Godehard A. Scholz, Sisi Xie, Tasneem Arsiwala, Daniel Guggisberg, Monique Vogel, Martin Bachmann and Burkhard Möller

Cells 2024, 13(21), 1792; https://doi.org/10.3390/cells13211792 - 29 Oct 2024

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Abstract

Background: In response to inflammation, the absorption of nutritional iron is restricted. Since the pathophysiological significance of the presence and uptake of iron in chronic inflammation is still unknown, we tested the effect of a low iron diet on the clinical course of [...] Read more.

Background: In response to inflammation, the absorption of nutritional iron is restricted. Since the pathophysiological significance of the presence and uptake of iron in chronic inflammation is still unknown, we tested the effect of a low iron diet on the clinical course of arthritis in the mouse model of collagen-induced arthritis (CIA). Methods: Six- to eight-week-old male DBA/1 mice were fed either a normal (51 mg/kg) or a low iron diet (5 mg/kg) starting four weeks before the first immunization. From day 4 after the second collagen booster made on day 25, the development of arthritis was regularly monitored until the end of the experiment (day 34), using a standard clinical arthritis score. Concentrations of mouse anti-bovine and anti-mouse collagen type 2 IgG antibodies were measured by ELISA; blood cell counts were performed and mediators of inflammation, tissue matrix degradation, oxygenation and oxidative stress were measured in the mouse sera of both diet groups at the end of the experiment by bead-based multiplex assay. Fe²⁺, Fe³⁺, oxidized and reduced glutathione (GSH and GSSG) and malondialdehyde (MDA) were quantified in whole paw tissue by ELISA. Quantitative PCR was performed in the tissues for glutathione peroxidase 4 and other key regulator genes of iron metabolism and ferroptosis. We used nonparametric tests to compare cross-sectional data. Nonlinear regression models were used for longitudinal data of the arthritis scores. Results: Mice fed a low iron diet showed a significantly less severe course of arthritis compared to mice fed a normal iron diet (p < 0.001). The immune response against bovine and mouse type 2 collagen did not differ between the two diet groups. Mice fed a low iron diet exhibited significantly lower serum levels of tissue inhibitor of metalloproteinase-1 (TIMP-1), a central regulator of inflammation and tissue matrix degradation (p < 0.05). In addition, a low iron diet led to a significant reduction in red blood cell indices, indicating restricted iron uptake and latent iron deficiency, but had no effect on hemoglobin concentrations or red blood cell counts. There were no differences between the dietary groups in Fe²⁺ or Fe³⁺ content in the paws. Based on calculation of the GSH/GSSG ratio and high MDA levels, high oxidative stress and lipid peroxidation were likewise detected in the paws of both diet groups of mice. Consequently, no differences associated with gene expression of key regulators of iron metabolism and ferroptosis could be detected between the paws of both diet groups. Conclusions: Restricted dietary iron intake alleviates immune-mediated inflammation in CIA without causing anemia. This finding suggests a promising option for dietary treatment of arthritis in inflammation. The underlying mechanism causing reduced arthritis may be linked to the complex regulatory network of TIMP-1 and appears to be independent from the local iron levels, oxidative stress and ferroptosis in the synovial tissues. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)

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Open AccessArticle

Reducing Oxidative Stress-Mediated Alcoholic Liver Injury by Multiplexed RNAi of Cyp2e1, Cyp4a10, and Cyp4a14

by Qi Zhang, Shuang Wu, Qiubing Chen, Yahong Zhang, Cai Zhang, Runting Yin, Zhen Ouyang and Yuan Wei

Biomedicines 2024, 12(7), 1505; https://doi.org/10.3390/biomedicines12071505 - 6 Jul 2024

Cited by 7 | Viewed by 2503

Abstract

The prevalence of excessive drinking-related alcoholic liver disease (ALD) is rising, yet therapeutic options remain limited. High alcohol consumption and consequent oxidative metabolism by cytochrome P450 (CYP) can lead to extremely high levels of reactive oxygen species, which overwhelm cellular defenses and harm [...] Read more.

The prevalence of excessive drinking-related alcoholic liver disease (ALD) is rising, yet therapeutic options remain limited. High alcohol consumption and consequent oxidative metabolism by cytochrome P450 (CYP) can lead to extremely high levels of reactive oxygen species, which overwhelm cellular defenses and harm hepatocytes. Our previous investigations showed that inhibiting Cyp2e1 using RNA interference reduced the incidence of ALD. However, compensatory mechanisms other than CYP2E1 contribute to oxidative stress in the liver. Therefore, we coupled triple siRNA lipid nanoparticles (LNPs) targeting Cyp2e1 with two isoenzymes Cyp4a10 and Cyp4a14 to treat ALD mouse models fed with Lieber–Decarli ethanol liquid diet for 12 weeks at the early (1st week), middle (5th week), and late (9th week) stages. The administration of triple siRNA LNPs significantly ameliorated chronic alcoholic liver injury in mice, and early treatment achieved the most profound effects. These effects can be attributed to a reduction in oxidative stress and increased expression of antioxidant genes, including Gsh-Px, Gsh-Rd, and Sod1. Moreover, we observed the alleviation of inflammation, evidenced by the downregulation of Il-1β, Il-6, Tnf-α, and Tgf-β, and the prevention of excessive lipid synthesis, evidenced by the restoration of the expression of Srebp1c, Acc, and Fas. Finally, triple siRNA treatment maintained normal metabolism in lipid oxidation. In brief, our research examined the possible targets for clinical intervention in ALD by examining the therapeutic effects of triple siRNA LNPs targeting Cyp2e1, Cyp4a10, and Cyp4a14. The in vivo knockdown of the three genes in this study is suggested as a promising siRNA therapeutic approach for ALD. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)

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15 pages, 4308 KiB  

Open AccessArticle

Therapeutic Effect of Donepezil on Neuroinflammation and Cognitive Impairment after Moderate Traumatic Brain Injury

by Dong Hyuk Youn, Younghyurk Lee, Sung Woo Han, Jong-Tae Kim, Harry Jung, Gui Seung Han, Jung In Yoon, Jae Jun Lee and Jin Pyeong Jeon

Life 2024, 14(7), 839; https://doi.org/10.3390/life14070839 - 1 Jul 2024

Cited by 3 | Viewed by 2465

Abstract

Background: Despite the important clinical issue of cognitive impairment after moderate traumatic brain injury (TBI), there is currently no suitable treatment. Here, we used in vitro and in vivo models to investigate the effect of Donepezil—an acetylcholinesterase (AChE) inhibitor—on cognitive impairment in the [...] Read more.

Background: Despite the important clinical issue of cognitive impairment after moderate traumatic brain injury (TBI), there is currently no suitable treatment. Here, we used in vitro and in vivo models to investigate the effect of Donepezil—an acetylcholinesterase (AChE) inhibitor—on cognitive impairment in the acute period following injury, while focusing on neuroinflammation and autophagy- and mitophagy-related markers. Methods: The purpose of the in vitro study was to investigate potential neuroprotective effects in TBI-induced cells after donepezil treatment, and the in vivo study, the purpose was to investigate therapeutic effects on cognitive impairment in the acute period after injury by analyzing neuroinflammation and autophagy- and mitophagy-related markers. The in vitro TBI model involved injuring SH-SY5Y cells using a cell-injury controller and then investigating the effect of donepezil at a concentration of 80 μM. The in vivo TBI model was made using a stereotaxic impactor for male C57BL/6J mice. Immuno-histochemical markers and cognitive functions were compared after 7 days of donepezil treatment (1 mg/kg/day). Mice were divided into four groups: sham operation with saline treatment, sham operation with donepezil treatment, TBI with saline treatment, and TBI with donepezil treatment (18 mice in each group). Donepezil treatment was administered within 4 h post-TBI. Results: In vitro, donepezil was found to lead to increased cell viability and 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimi-dazolylcarbocyanine iodide (JC-1), along with decreased reactive oxygen species (ROS), lactate-dehydrogenase (LDH), 2′-7′-dichlorodihydrofluorescein diacetate (DCFH-DA)-positive cells, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells. The mRNA and protein expressions of neuroinflammation (Cyclooxygenase-2, COX-2; NOD-like receptor protein 3, NLRP3; Caspase-1; and Interleukin-1 beta, IL-1β), as well as autophagy- and mitophagy-related markers (death-associated protein kinase 1, DAPK1; PTEN-induced kinase 1, PINK1; BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like, BNIP3L; Beclin-1, BECN1; BCL2-associated X protein, BAX; microtubule-associated protein 1A/1B-light chain 3B (LC3B); Sequestosome-1; and p62) were all found to decrease after donepezil treatment. The in vivo study also showed that donepezil treatment resulted in decreased levels of cortical tissue losses and brain swelling in TBI compared to the TBI group without donepezil treatment. Donepezil treatment was also shown to decrease the mRNA and Western blotting expressions of all markers, and especially COX-2 and BNIP3L, which showed the most significant decreases. Moreover, TBI mice showed an decreased escape latency, increased alteration rate, and improved preference index, altogether pointing to better cognitive performance after donepezil treatment. Conclusions: Donepezil treatment may be beneficial in improving cognitive impairment in the early phase of moderate traumatic brain injury by ameliorating neuroinflammation, as well as autophagy and mitophagy. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)

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13 pages, 1887 KiB  

Open AccessArticle

Protective Effect of Hyperprolactinemia on Oxidative Stress in Patients with Psychotic Disorder on Atypical Antipsychotics Risperidone and Paliperidone: A Cross-Sectional Study

by Milena Stojkovic, Mirjana Jovanovic, Vladimir Jakovljevic, Vladimir Zivkovic, Natasa Djordjevic, Aleksandar Kocovic, Marina Nikolic, Aleksandra Stojanovic, Natasa Minic, Vesna Ignjatovic, Vladimir Vukomanovic, Danijela Nastic, Natasa Zdravkovic, Olivera Radmanovic, Milan Djordjic, Sasa Babic and Branimir Radmanovic

Biomedicines 2024, 12(7), 1418; https://doi.org/10.3390/biomedicines12071418 - 26 Jun 2024

Cited by 1 | Viewed by 1522

Abstract

Several studies indicate the impact of antipsychotics like risperidone and paliperidone on oxidative stress parameters, yet data remain inconsistent. We investigated the link between these medications, hyperprolactinemia (HPRL), and oxidative stress. This study was conducted at the Psychiatry Clinic, University Clinical Center, Kragujevac, [...] Read more.

Several studies indicate the impact of antipsychotics like risperidone and paliperidone on oxidative stress parameters, yet data remain inconsistent. We investigated the link between these medications, hyperprolactinemia (HPRL), and oxidative stress. This study was conducted at the Psychiatry Clinic, University Clinical Center, Kragujevac, between November 2022 and August 2023. Inclusion criteria comprised diagnosed psychotic disorders from the ICD-10-based F20-F29 spectrum and clinical stability on risperidone/paliperidone for ≥12 weeks with no recent dose adjustments. Exclusion criteria included pregnancy, breastfeeding, relevant medical conditions, or co-therapy with prolactin-secreting drugs. Data encompassed drug choice, administration method, therapy duration, and daily dose. Prolactin (PRL) levels, oxidative stress parameters (TBARS, H₂O₂, O₂⁻, NO₂⁻), and antioxidant system (CAT, GSH, SOD) were assessed. Of 155 subjects, women exhibited significantly higher PRL levels (p < 0.001) and symptomatic HPRL (p < 0.001). Drug choice and regimen significantly influenced TBARS (p < 0.001), NO₂⁻ (p < 0.001), O₂⁻ (p = 0.002), CAT (p = 0.04), and GSH (p < 0.001) levels. NO₂⁻ levels were affected by drug dose (p = 0.038). TBARS (p < 0.001), O₂⁻ (p < 0.001), and SOD (p = 0.022) inversely correlated with PRL levels, suggesting PRL’s protective role against oxidative stress. The female sex association with higher PRL levels implies additional factors influencing PRL’s antioxidant role. Antipsychotic choice and dosage impact PRL and oxidative stress markers, necessitating further exploration. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)

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22 pages, 3076 KiB  

Open AccessArticle

A Nonclinical Safety Evaluation of Cold Atmospheric Plasma for Medical Applications: The Role of Genotoxicity and Mutagenicity Studies

by Piimwara Yarangsee, Supakit Khacha-ananda, Pornsiri Pitchakarn, Unchisa Intayoung, Sirikhwan Sriuan, Jirarat Karinchai, Apiwat Wijaikhum and Dheerawan Boonyawan

Life 2024, 14(6), 759; https://doi.org/10.3390/life14060759 - 13 Jun 2024

Cited by 2 | Viewed by 1451

Abstract

Atmospheric nonthermal plasma (ANTP) has rapidly evolved as an innovative tool in biomedicine with various applications, especially in treating skin diseases. In particular, the formation of reactive oxygen species (ROS) and nitrogen species (RNS), which are generated by ANTP, plays an important role [...] Read more.

Atmospheric nonthermal plasma (ANTP) has rapidly evolved as an innovative tool in biomedicine with various applications, especially in treating skin diseases. In particular, the formation of reactive oxygen species (ROS) and nitrogen species (RNS), which are generated by ANTP, plays an important role in the biological signaling pathways of human cells. Unfortunately, excessive amounts of these reactive species significantly result in cellular damage and cell death induction. To ensure the safe application of ANTP, preclinical in vitro studies must be conducted before proceeding to in vivo or clinical trials involving humans. Our study aimed to investigate adverse effects on genetic substances in murine fibroblast cells exposed to ANTP. Cell viability and proliferation were markedly reduced after exposing the cells with plasma. Both extracellular and intracellular reactive species, especially RNS, were significantly increased upon plasma exposure in the culture medium and the cells. Notably, significant DNA damage in the cells was observed in the cells exposed to plasma. However, plasma was not classified as a mutagen in the Ames test. This suggested that plasma led to the generation of both extracellular and intracellular reactive species, particularly nitrogen species, which affect cell proliferation and are also known to induce genetic damage in fibroblast cells. These results highlight the genotoxic and mutagenic effects of ANTP, emphasizing the need for the cautious selection of plasma intensity in specific applications to avoid adverse side effects resulting from reactive species production. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)

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17 pages, 5450 KiB  

Open AccessArticle

Saliva as a Diagnostic Tool for Early Detection of Exercise-Induced Oxidative Damage in Female Athletes

by Aleksandr N. Ovchinnikov and Antonio Paoli

Biomedicines 2024, 12(5), 1006; https://doi.org/10.3390/biomedicines12051006 - 2 May 2024

Cited by 1 | Viewed by 2131

Abstract

Although blood still remains the most commonly utilized medium to detect increased levels of oxidative damage induced by exercise, saliva diagnostics have gained increasing popularity due to their non-invasive nature and athlete-friendly collection process. Given that the contribution of various phases of the [...] Read more.

Although blood still remains the most commonly utilized medium to detect increased levels of oxidative damage induced by exercise, saliva diagnostics have gained increasing popularity due to their non-invasive nature and athlete-friendly collection process. Given that the contribution of various phases of the menstrual cycle to the levels of oxidative damage may differ, the aim of this study was to evaluate an agreement between salivary and plasmatic levels of lipid peroxidation products in female swimmers in both the follicular (F) and luteal (L) phases of the menstrual cycle at rest and following exercise. Twelve well-trained female swimmers aged 19.6 ± 1.1 years old were examined. We measured diene conjugates (DCs), triene conjugates (TCs), and Schiff bases (SBs) in lipids immediately after their extraction from both saliva and blood plasma. All female swimmers were studied two times each, in the two different phases of one menstrual cycle, before and after high-intensity interval exercise (HIIE). Salivary and plasmatic levels of DCs, TCs, and SBs significantly increased post-exercise compared to pre-exercise, in both the F and L phases. A high positive correlation was observed between the concentrations of DCs, TCs, and SBs in the saliva and blood plasma of participants in the F and L phases, both at rest and following HIIE. Ordinary least products regression analysis indicates that there was no proportional and differential bias in the data. The Bland–Altman method also declares that there was no differential bias, since the line of equality was within the 95% confidence interval of the mean difference between salivary and plasmatic levels of DCs, TCs, and SBs in female swimmers, in both the F and L phases, before and after HIIE. There was also no proportional bias in the Bland–Altman plots. Thus, this is the first study to report a high agreement between the quantifications of DCs, TCs, and SBs in the saliva and blood plasma of female swimmers in both the F and L phases, at rest and following HIIE. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)

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Open AccessArticle

Human Macrophages Activate Bystander Neutrophils’ Metabolism and Effector Functions When Challenged with Mycobacterium tuberculosis

by Dearbhla M. Murphy, Anastasija Walsh, Laura Stein, Andreea Petrasca, Donal J. Cox, Kevin Brown, Emily Duffin, Gráinne Jameson, Sarah A. Connolly, Fiona O’Connell, Jacintha O’Sullivan, Sharee A. Basdeo, Joseph Keane and James J. Phelan

Int. J. Mol. Sci. 2024, 25(5), 2898; https://doi.org/10.3390/ijms25052898 - 1 Mar 2024

Cited by 2 | Viewed by 3293

Abstract

Neutrophils are dynamic cells, playing a critical role in pathogen clearance; however, neutrophil infiltration into the tissue can act as a double-edged sword. They are one of the primary sources of excessive inflammation during infection, which has been observed in many infectious diseases [...] Read more.

Neutrophils are dynamic cells, playing a critical role in pathogen clearance; however, neutrophil infiltration into the tissue can act as a double-edged sword. They are one of the primary sources of excessive inflammation during infection, which has been observed in many infectious diseases including pneumonia and active tuberculosis (TB). Neutrophil function is influenced by interactions with other immune cells within the inflammatory lung milieu; however, how these interactions affect neutrophil function is unclear. Our study examined the macrophage–neutrophil axis by assessing the effects of conditioned medium (MΦ-CM) from primary human monocyte-derived macrophages (hMDMs) stimulated with LPS or a whole bacterium (Mycobacterium tuberculosis) on neutrophil function. Stimulated hMDM-derived MΦ-CM boosts neutrophil activation, heightening oxidative and glycolytic metabolism, but diminishes migratory potential. These neutrophils exhibit increased ROS production, elevated NET formation, and heightened CXCL8, IL-13, and IL-6 compared to untreated or unstimulated hMDM-treated neutrophils. Collectively, these data show that MΦ-CM from stimulated hMDMs activates neutrophils, bolsters their energetic profile, increase effector and inflammatory functions, and sequester them at sites of infection by decreasing their migratory capacity. These data may aid in the design of novel immunotherapies for severe pneumonia, active tuberculosis and other diseases driven by pathological inflammation mediated by the macrophage–neutrophil axis. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)

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22 pages, 18029 KiB  

Open AccessArticle

Reactive Oxygen Species-Dependent Activation of EGFR/Akt/p38 Mitogen-Activated Protein Kinase and JNK1/2/FoxO1 and AP-1 Pathways in Human Pulmonary Alveolar Epithelial Cells Leads to Up-Regulation of COX-2/PGE₂ Induced by Silica Nanoparticles

by Yan-Jyun Lin, Chien-Chung Yang, I-Ta Lee, Wen-Bin Wu, Chih-Chung Lin, Li-Der Hsiao and Chuen-Mao Yang

Biomedicines 2023, 11(10), 2628; https://doi.org/10.3390/biomedicines11102628 - 25 Sep 2023

Cited by 7 | Viewed by 2250

Abstract

The risk of lung exposure to silica nanoparticles (SiNPs) and related lung inflammatory injury is increasing with the wide application of SiNPs in a variety of industries. A growing body of research has revealed that cyclooxygenase (COX)-2/prostaglandin E₂ (PGE₂) up-regulated [...] Read more.

The risk of lung exposure to silica nanoparticles (SiNPs) and related lung inflammatory injury is increasing with the wide application of SiNPs in a variety of industries. A growing body of research has revealed that cyclooxygenase (COX)-2/prostaglandin E₂ (PGE₂) up-regulated by SiNP toxicity has a role during pulmonary inflammation. The detailed mechanisms underlying SiNP-induced COX-2 expression and PGE₂ synthesis remain unknown. The present study aims to dissect the molecular components involved in COX-2/PGE₂ up-regulated by SiNPs in human pulmonary alveolar epithelial cells (HPAEpiCs) which are one of the major targets while SiNPs are inhaled. In the present study, we demonstrated that SiNPs induced COX-2 expression and PGE₂ release, which were inhibited by pretreatment with a reactive oxygen species (ROS) scavenger (edaravone) or the inhibitors of proline-rich tyrosine kinase 2 (Pyk2, PF-431396), epidermal growth factor receptor (EGFR, AG1478), phosphatidylinositol 3-kinase (PI3K, LY294002), protein kinase B (Akt, Akt inhibitor VIII), p38 mitogen-activated protein kinase (MAPK) (p38 MAPK inhibitor VIII), c-Jun N-terminal kinases (JNK)1/2 (SP600125), Forkhead Box O1 (FoxO1, AS1842856), and activator protein 1 (AP-1, Tanshinone IIA). In addition, we also found that SiNPs induced ROS-dependent Pyk2, EGFR, Akt, p38 MAPK, and JNK1/2 activation in these cells. These signaling pathways induced by SiNPs could further cause c-Jun and FoxO1 activation and translocation from the cytosol to the nucleus. AP-1 and FoxO1 activation could increase COX-2 and PGE₂ levels induced by SiNPs. Finally, the COX-2/PGE₂ axis might promote the inflammatory responses in HPAEpiCs. In conclusion, we suggested that SiNPs induced COX-2 expression accompanied by PGE₂ synthesis mediated via ROS/Pyk2/EGFR/PI3K/Akt/p38 MAPK- and JNK1/2-dependent FoxO1 and AP-1 activation in HPAEpiCs. Full article

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Open AccessArticle

Chlorogenic Acid Alleviates LPS-Induced Inflammation and Oxidative Stress by Modulating CD36/AMPK/PGC-1α in RAW264.7 Macrophages

by Tiantian Gu, Zhiguo Zhang, Jinyu Liu, Li Chen, Yong Tian, Wenwu Xu, Tao Zeng, Weicheng Wu and Lizhi Lu

Int. J. Mol. Sci. 2023, 24(17), 13516; https://doi.org/10.3390/ijms241713516 - 31 Aug 2023

Cited by 25 | Viewed by 3133

Abstract

Chlorogenic acid (CGA) is a bioactive substance with anti-inflammatory activities. Clusters of CD36 have been suggested to be widely involved in inflammatory damage. However, the mechanism of CGA protecting against LPS-induced inflammation involving the CD36 regulation is unclear. Here, we demonstrated that CGA [...] Read more.

Chlorogenic acid (CGA) is a bioactive substance with anti-inflammatory activities. Clusters of CD36 have been suggested to be widely involved in inflammatory damage. However, the mechanism of CGA protecting against LPS-induced inflammation involving the CD36 regulation is unclear. Here, we demonstrated that CGA protected against LPS-induced cell death and decreased the production of ROS. Moreover, the SOD, CAT, and GSH-Px activities were also upregulated in CGA-treated cells during LPS stimulation. CGA reduced COX-2 and iNOS expression and IL-1β, IL-6, and TNF-α secretion in LPS-stimulated RAW264.7 macrophages. In addition, CGA treatment widely involved in immune-related signaling pathways, including NF-κB signaling, NOD-like receptor signaling, and IL-17 signaling using transcriptomic analysis and CD36 also markedly reduced during CGA pretreatment in LPS-induced RAW264.7 cells. Furthermore, the CD36 inhibitor SSO attenuated inflammation and oxidative stress by enabling activation of the AMPK/PGC-1α cascade. These results indicate that CGA might provide benefits for the regulation of inflammatory diseases by modulating CD36/AMPK/PGC-1α to alleviate oxidative stress. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)

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16 pages, 1024 KiB  

Open AccessReview

Antioxidant Therapy as an Effective Strategy against Noise-Induced Hearing Loss: From Experimental Models to Clinic

by Anna Pisani, Fabiola Paciello, Raffaele Montuoro, Rolando Rolesi, Jacopo Galli and Anna Rita Fetoni

Life 2023, 13(4), 1035; https://doi.org/10.3390/life13041035 - 17 Apr 2023

Cited by 10 | Viewed by 6174

Abstract

Cochlear redox unbalance is the main mechanism of damage involved in the pathogenesis of noise-induced-hearing loss. Indeed, the increased free radical production, in conjunction with a reduced efficacy of the endogenous antioxidant system, plays a key role in cochlear damage induced by noise [...] Read more.

Cochlear redox unbalance is the main mechanism of damage involved in the pathogenesis of noise-induced-hearing loss. Indeed, the increased free radical production, in conjunction with a reduced efficacy of the endogenous antioxidant system, plays a key role in cochlear damage induced by noise exposure. For this reason, several studies focused on the possibility to use exogenous antioxidant to prevent or attenuate noise-induce injury. Thus, several antioxidant molecules, alone or in combination with other compounds, have been tested in both experimental and clinical settings. In our findings, we tested the protective effects of several antioxidant enzymes, spanning from organic compounds to natural compounds, such as nutraceuticals of polyphenols. In this review, we summarize and discuss the strengths and weaknesses of antioxidant supplementation focusing on polyphenols, Q-Ter, the soluble form of CoQ10, Vitamin E and N-acetil-cysteine, which showed great otoprotective effects in different animal models of noise induced hearing loss and which has been proposed in clinical trials. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 2nd Volume)

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