Epilepsy is a neurological brain disease characterized by multiple seizures with short intervals and becomes drug-resistant when it causes oxidative stress and inflammation in the brain. Ferulic acid (FA) is a plant phenolic substance with antioxidant, anti-inflammatory, and neuroprotective effects that is used in the treatment of neurodegenerative diseases in traditional medicine. This study evaluated the effect of FA (20 or 80 mg/kg) alone and then FA (20 mg/kg) combined with valproate (VPA) or carbamazepine (CBZ) on maximal electroshock-induced seizures (MESs) in mice associated with interleukin-1β (IL-1β) concentrations and total antioxidant capacity (TAC) assessment in the hippocampus. Male NMRI mice (weight 25-30 g) were injected intraperitoneally with saline (1 mL/kg), FA (20 or 80 mg/kg), diazepam (D) (20 mg/kg), VPA (200 mg/kg), CBZ (10 mg/kg), FA (20 mg/kg) + VPA (200 mg/kg), and FA (20 mg/kg) + CBZ (10 mg/kg) before application of MES. Duration of tonic hind limb extension (HLE), and chimney climbing time and grip-strength were also recorded. Then, mice scarified and hippocampus removed and homogenized. The level of IL-1β and TAC were determined. FA (20 and 80 mg/kg) significantly reduced the HLE duration and prevented seizure-induced hippocampal IL-1β increase and antioxidant capacity decrease. In addition, FA (20 mg/kg) enhanced the anticonvulsant efficacy of VPA and CBZ by regulating hippocampal IL-1β and antioxidant capacity. The finding suggest that FA possessed anticonvulsant effect and improved VPA and CBZ efficacy by regulating of IL-1β and antioxidant capacity in the hippocampus.

[This retracts the article DOI: 10.1155/2020/6501294.].

[This retracts the article DOI: 10.1155/2021/3417242.].

[This corrects the article DOI: 10.1155/2022/5491038.].

Doxorubicin (Doxo) is an anthracycline widely used as a chemotherapeutic agent for many solid and hematological cancers. Its clinical use is limited due to a cumulative dose-dependent and irreversible cardiotoxicity that can cause progressive cardiomyopathy and congestive heart failure. A cardioprotective therapy that can decrease heart damage without reducing the anticancer efficacy during Doxo therapy is of utmost importance. Anthocyanins (ACNs) are renowned cardioprotective agents thanks to their antioxidant and anti-inflammatory properties. An ACN-rich diet from purple corn, which mainly contains cyanidin 3-glucoside (C3G) and its acetylated derivatives, has been previously shown to be effective in reducing Doxo-induced cardiotoxicity in mice. Aiming at unveiling the molecular mechanisms involved in ACN protection, we considered the fibroblast growth factor 21/AMP-activated protein kinase/SIRTUIN1 (FGF21/AMPK/SIRT1)/p53 pathway in murine HL-1 cardiomyocytes treated with Doxo in the presence or absence of purple corn extract (RED). Our work shows that Doxo-induced AMPK activation is restored to control levels by the RED extract. p53 acetylation was increased by the RED extract and upon Sirt1 silencing, indicating that p53 acetylation is SIRT1-dependent and suggesting that the RED extract may affect SIRT1 activity through AMPK. Notably, increased p53 acetylation led to decreased levels of cleaved-caspase 3 and Puma and p21 transcript levels, indicating a reduced level of apoptosis. The RED-induced cardioprotection and p53 acetylation were confirmed in mouse primary cardiomyocytes. In conclusion, the RED extract may prevent cardiomyocytes apoptosis through the modulation of AMPK and acetylation of p53.

[This corrects the article DOI: 10.1155/2019/5972575.].

[This retracts the article DOI: 10.1155/2018/4501097.].

[This corrects the article DOI: 10.1155/2021/9970272.].

[This retracts the article DOI: 10.1155/2020/8026838.].

[This retracts the article DOI: 10.1155/2023/6916819.].

Obesity-associated metabolic dysfunction is closely linked to chronic low-grade inflammation, or metaflammation, which is predominantly driven by changes in AT homeostasis. Macrophages, key components of the innate immune system, are central regulators of this inflammatory process. In lean AT, resident macrophages (AT-associated macrophages [ATMs]) exhibit an anti-inflammatory phenotype and support tissue homeostasis. However, during obesity, AT undergoes hypoxia, mechanical stress, and lipid overload, leading to immune cell infiltration and a phenotypic switch of ATMs toward a proinflammatory M1 profile. This shift contributes to systemic inflammation and obesity-associated metabolic risks. Here, we review the current understanding of macrophage polarization in obesity, highlighting the transcriptomic plasticity and functional heterogeneity of ATMs, their interactions within the AT microenvironment, and the formation of crown-like structures (CLSs) as a structural hallmark of AT inflammation. We also discuss the regulatory functions of transcription factors, such as hypoxia-inducible factor (HIF) 1α (HIF-1α) and peroxisome proliferator activated receptor gamma (PPARγ), that control the phenotypic switch of macrophages in healthy and obese ATs. Furthermore, we examined emerging macrophage subsets, such as CD9 and Trem2 lipid-associated macrophages (LAMs), and their dual roles in AT remodeling and inflammation. Understanding the complex network of macrophage activation in obese AT is essential for identifying therapeutic targets aimed at mitigating obesity-associated metabolic risk and restoring tissue function.

Oxidative stress plays a crucial role in the pathogenesis of preeclampsia. Given that the NADPH quinone oxidoreductase 1 (NQO1) is an important enzyme in the antioxidant system, this study aimed to investigate the relationship between the NQO1 rs1800566 polymorphism, NQO1 promoter methylation, and oxidative stress with the risk of preeclampsia.

[This retracts the article DOI: 10.1155/2017/1206420.].

[This retracts the article DOI: 10.1155/2023/4256116.].

[This corrects the article DOI: 10.1155/2022/7038834.].

Pulmonary neutrophilic inflammation (PNI) is the recruitment and activation of neutrophils in the microvasculature with the release of myeloperoxidase (MPO) in the airways. Bystander epithelial cells can take up MPO, where it can generate HOCl. HOCl can react with DNA, generating DNA radicals, which then decay to produce several mutagenic end-oxidation products, such as 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxo-dGuo). Herein, we aimed to test whether HOCl-induced DNA radicals precede DNA oxidation and mutagenesis in A549 human lung epithelial cells as an in vitro model that resembles PNI. Interestingly, by trapping HOCl-induced DNA radicals, the nitrone spin trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO) blocks the formation of 8-oxo-dGuo and possibly other end-oxidation products, forming DNA-DMPO nitrone adducts. By preventing DNA oxidation, DMPO reduces the mutation of the hypoxanthine phosphoribosyl transferase () gene, one of the genes most sensitive to oxidative damage. The transcription factor p53 is known as the master regulator of the cell response to genomic damage. By trapping DNA radicals, DMPO also blocks the translocation of p53 to the cell nucleus, suggesting that by trapping DNA radicals with DMPO, end-oxidation products are prevented, and the cell response to genomic damage is blunted. Trapping DNA radicals to reduce the accumulation of HOCl-induced mutagenic end-oxidation products will provide new therapeutic avenues to reduce genotoxic damage during PNI.

[This corrects the article DOI: 10.1155/2021/2860488.].

Exposure to hyperoxia lasting either a few days at normobaria or a few hours at hyperbaria induces pulmonary oxygen toxicity. Cellular functional changes resulting from oxygen toxicity include alterations in both mitochondrial dynamics and bioenergetics. The primary goal of this study was to quantify the prophylactic effects of three compounds, caffeine, MitoQ, and γ-aminobutyric acid (GABA), to protect human pulmonary cells in vitro from mitochondrial alterations induced by normobaric- and hyperbaric-hyperoxic conditions. Using cultured lung microvascular and pulmonary artery endothelial cells as well as A549 cells, we examined mitochondrial dynamic and bioenergetics function following exposure to normobaric-hyperoxic (5% CO and 95% O for 72 h) and hyperbaric-hyperoxic (~5% CO equivalent and remainder O at pressure of 4.8 atmosphere absolute (ATA) for 4 h) conditions in the presence of the drugs. Mitochondrial respiration parameters, inner membrane potential, motility, intracellular distribution, and size were measured, along with quantitation of respiration complex levels. Redistribution of intracellular ATP-linked respiration was determined. Comparisons of results were made to controls under normobaric-normoxic conditions. Effects of the drugs under control conditions were also measured. Presence of the drugs resulted in differential effects on hyperoxia-induced alterations in cellular respiration function, stability of mitochondrial potential, and distribution of ATP-linked respiration within the cell. Inclusion of these drugs also produced unique signatures for respiration complex protein levels. Moreso for caffeine than for MitoQ and GABA, its inclusion in the face of hyperoxic exposure served to preserve mitochondrial bioenergetics function, primarily by promoting intracellular redistribution of mitochondrial volume to the perinuclear space. These results indicate a potential role for pharmacologic prophylaxis via therapeutics targeted to support mitochondrial function as a means of protecting the lung from hyperoxia-induced pulmonary cellular oxygen toxicity.

[This retracts the article DOI: 10.1155/2021/4704771.].

[This retracts the article DOI: 10.1155/2022/7202837.].

[This retracts the article DOI: 10.1155/2021/3672112.].