Soluble E‐cadherin is associated with oxidative stress in patients with chronic HBV infection

Yang, Jun; Xiong, Yuan; Zhou, Lijin; Huang, Yong; Chen, Weixian; Wang, Bo

doi:10.1002/jmv.25571

Cited by 8 publications

(7 citation statements)

References 33 publications

(38 reference statements)

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“…As a product of lipid peroxidation, MDA level can reflect the degree of lipid peroxidation in oxidative damage to a certain extent. 38 In this experiment, rainfrog peptide significantly reduced the activity of SOD and GSH, increased the production of ROS, thus increasing the death of pancreatic acinar cells and decreasing the cell apoptosis. After baicalin treatment, the activities of SOD and GSH were increased, the production of ROS was decreased.…”

Section: Discussionmentioning

confidence: 73%

“…MiR-136 promotes LPS-induced ATDC5 cell damage and inflammatory cytokine expression by targeting myeloid leukemia 1. 38 Overexpressed Mir-136-5p inhibited the expression of A20 protein and promoted the production of inflammatory factors, chemokines, and P-NF-kB in rats with acute spinal cord injury. It also increased the infiltration and injury of inflammatory cells in the spinal cord.…”

Section: Discussionmentioning

confidence: 99%

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Protective effects of baicalin on caerulein-induced AR42J pancreatic acinar cells by attenuating oxidative stress through miR-136-5p downregulation

et al. 2021

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Baicalin, the main active component of Scutellaria baicalensis, has antioxidant and anti-apoptotic effects and is used to treat acute pancreatitis; however, its specific mechanism is unclear. This study aims to determine the protective effect and underlying mechanism of baicalin on AR42J pancreatic acinar cell injury. AR42J acinar cells (caerulein, 10 nmol/L) were induced in vitro to establish a cell model for acute pancreatitis. Cell relative survival was measured by thiazolyl blue tetrazolium bromide, and cell apoptosis and death were examined by flow cytometry. The expression levels of superoxide dismutase1 (SOD1), Bax, survivin, Bcl-2, caspase-3, and caspase-7 proteins were analyzed by Western blot, and those of SOD1 mRNA and miR-136-5p were determined by RT-PCR. The activities of GSH, SOD1, ROS, and MDA were also investigated. Compared with those of the caerulein group, the relative survival rate and activity of AR42J pancreatic acinar cells with different baicalin concentrations were significantly increased ( p < 0.05), and the supernatant amylase level was markedly decreased ( p < 0.05). In addition, the ROS and MDA activities and mir-136-5p expression were significantly decreased, and the GSH activities and SOD1 gene and protein expression levels were markedly increased ( p < 0.05). These results suggest that baicalin reduced the caerulein-induced death of AR42J acinar cells and alleviated the caerulein-induced injury in pancreatic acinar cells by inhibiting oxidative stress. The mechanism may be related to the decreased expression of Mir-136-5p and the increased expression of SOD1 gene and protein.

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Section: Discussionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Protective effects of baicalin on caerulein-induced AR42J pancreatic acinar cells by attenuating oxidative stress through miR-136-5p downregulation

et al. 2021

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“…Urinary E-cadherin emerges as a specific marker for diabetic kidney injury (65). Recent findings also link E-cadherin to inflammation and oxidative stress in chronic hepatitis B virus (66). Regarding NS, limited research exists, with a single study revealing lower urinary E-cadherin in the acute phase versus remission (31).…”

Section: Discussionmentioning

confidence: 99%

Pediatric nephrotic syndrome: The interplay of oxidative stress and inflammation

Mulat,

Mihajlović,

Antonić

et al. 2024

J Med Biochemistry

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Summary Background: The pathophysiological mechanisms crucial in the development of nephrotic syndrome (NS) in the pediatric population are still not fully understood. This study aims to investigate the synergistic interaction of oxidative stress and inflammation in the pathogenesis of NS. Additionally, one of the objectives of this study is to examine the relationship between hypertension and the degree of oxidative stress and inflammation in patients during the acute phase of the disease. Methods: The study included 33 children, aged 2 to 9 years, with NS. Blood samples were collected during the acute phase and remission. Parameters of oxidative status were determined, including total oxidative status (TOS), advanced oxidation protein products (AOPP), prooxidant-antioxidant balance (PAB), sulfhydryl groups (-SH), paraoxonase 1 (PON1), and total antioxidant status (TAS) in serum, measured spectrophotometrically. Inflammatory parameters such as pentraxin 3 (PTX3), leptin, programmed cell death ligand 1 (PD-L1), and E-cadherin were determined using enzyme-linked immunosorbent assay (ELISA). Results: Patients with NS and hypertension had significantly higher levels of AOPP and TOS (p=0.029 and p=0.003, respectively). During the acute phase of the disease, lower activity of -SH and PON1 was observed compared to remission (p<0.001, for both). PTX3 levels were higher, while leptin levels were lower during the acute phase (p<0.001, for both). PTX3 correlated with AOPP and TAS during the acute phase but not in remission (rs=0.42, p=0.027 and rs=0.43, p=0.025, respectively). A negative correlation between AOPP and leptin was observed during the acute phase, which disappeared in remission (rs=-0.42, p=0.028). Conclusions: Results of this study show that hypertension influences oxidative stress markers, and decreased antioxidant capacity may contribute to NS development. PTX 3 appears as a potential disease activity marker, indicating a dynamic connection between inflammation and oxidative stress. Leptin may also play a role in oxidative stress in NS. List of abbreviations: AOPP, advanced oxidation protein products; BMI, body mass index; DBP, diastolic blood pressure; ELISA, enzyme-linked immunosorbent assay; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; total antioxidant status; PAB, prooxidant-antioxidant balance; -SH, sulfhydryl group; SBP, systolic blood pressure; PON 1, paraoxonase; PTX 3, pentraxin 3; PD-L1, programmed cell death ligand 1; TC, total cholesterol; TG, triglyceride; TAS, total antioxidant status; TOS, total oxidation status.

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“…Reduction of organic peroxides to alcohols: ROOH + 2GSH → ROH + GSSG + H 2 O 4. Isomerization (steroids, prostaglandins) (Yang et al, 2020).…”

Section: Glutathione Transferasementioning

confidence: 99%

Oxidative stress and disruption of the antioxidant defense system as triggers of diseases

Skoryk,

Horila

2023

Regul. Mech. Biosyst.

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Oxidative stress is a state when the content of free radicals in a living organism is excessive. Molecules of free radical nature start a chain reaction that disrupts the integrity of cells, leading to their damage or death. The article examines the issue of intensification of oxidative stress processes and changes in the antioxidant defense system during the occurrence, development, and treatment of diseases of various etiologies. The principles of antioxidant/prooxidant balance regulation at the physiological and biochemical levels in living organisms are discussed. It was determined that the phenomenon of oxidative stress, as a completely special type of stress, is mediated by free radicals that have a destructive effect on the membranes of living cells. Free radical molecules are damaging agents for nucleic acids, proteins and lipids. The leading role in biological systems is played by oxygen free radicals, namely superoxide anion. The system of antioxidant protection, which prevents the harmful effects of oxidative stress on living organisms, is described in detail. The work describes the components of the antioxidant protection system, such as electron acceptors – vitamins E and K3; acceptors of superoxide radical anions – methionine, cysteine; scavengers of hydroxyl radicals – aliphatic alcohols; factors for detoxification of toxic products of lipid peroxidation, tocopherol, ionol, superoxide dismutase, glutathione peroxidase system, chelators of metals with variable valence (complexons) and others. According to the nature and mechanism of action, antioxidant protection agents are divided into hydrophilic and hydrophobic, enzymatic (catalase, superoxide dismutase, glutathione peroxidase system, glutathione, ascorbic acid, adrenaline, serotonin, tocopherols, retinoids, flavonoids, phospholipids, ceruloplasmin) and non-enzymatic factors. It is noted that in the human body, oxidative stress is the cause or an important component of many serious diseases, such as oncological pathologies, neurodegenerative processes (atherosclerosis and Alzheimer’s disease), diseases of the gastrointestinal tract, as well as aging. Although in some cases, oxidative stress can act as a protective mechanism in the body. Thus, the human immune system uses oxidative stress to fight pathogens, and some reactive oxygen species can serve as mediators in signal transmission during the immune response. Therefore, the biochemical mechanism of the development of many diseases of different etiology is closely related to disturbances in the antioxidant defense system and the occurrence of oxidative stress.

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Soluble E‐cadherin is associated with oxidative stress in patients with chronic HBV infection

Cited by 8 publications

References 33 publications

Protective effects of baicalin on caerulein-induced AR42J pancreatic acinar cells by attenuating oxidative stress through miR-136-5p downregulation

Protective effects of baicalin on caerulein-induced AR42J pancreatic acinar cells by attenuating oxidative stress through miR-136-5p downregulation

Pediatric nephrotic syndrome: The interplay of oxidative stress and inflammation

Oxidative stress and disruption of the antioxidant defense system as triggers of diseases

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