Neuroprotective effects of oxymatrine on hypoxic–ischemic brain damage in neonatal rats by activating the Wnt/β-catenin pathway

Lan, Xiao-Bing; Ni, Yuan-Shu; Liu, Ning; Wei, Wei; Liu, Yue; Yang, Jiamei; Ma, Lin; Bai, Ruixiang; Zhang, Jian; Yu, Jian‐Qiang

doi:10.1016/j.biopha.2023.114266

Cited by 9 publications

(7 citation statements)

References 53 publications

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“…Astaxanthin also protected mitochondrial function against oxidative injury induced by H 2 O 2 , leading to the significant recovery of mitochondrial membrane potential (Figure 1C) and preventing a decrease in the adenosine triphosphate (ATP) level (Figure 1D). Neuronal apoptosis is a major pathological process associated with neuro function in neurons after external stimulation [26]. Hoechst 33258 staining [2 ployed to examine whether H2O2 induced apoptosis.…”

Section: Effects Of Astaxanthin On Cell Survival Mitochondrial Functi...mentioning

confidence: 99%

“…These results indicate t thin might repress apoptosis induced by H2O2 in SH-SY5Y cells by regulatin signals. Neuronal apoptosis is a major pathological process associated with neurological dysfunction in neurons after external stimulation [26]. Hoechst 33258 staining [27] was employed to examine whether H 2 O 2 induced apoptosis.…”

Section: Effects Of Astaxanthin On Cell Survival Mitochondrial Functi...mentioning

confidence: 99%

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Astaxanthin Inhibits H2O2-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR Activation

Yan,

Ding,

Zhang

et al. 2024

Marine Drugs

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Oxidative stress, which damages cellular components and causes mitochondrial dysfunction, occurs in a variety of human diseases, including neurological disorders. The clearance of damaged mitochondria via mitophagy maintains the normal function of mitochondria and facilitates cell survival. Astaxanthin is an antioxidant known to have neuroprotective effects, but the underlying mechanisms remain unclear. This study demonstrated that astaxanthin inhibited H2O2-induced apoptosis in SH-SY5Y cells by ameliorating mitochondrial damage and enhancing cell survival. H2O2 treatment significantly reduced the levels of activated Akt and mTOR and induced mitophagy, while pretreatment with astaxanthin prevented H2O2-induced inhibition of Akt and mTOR and attenuated H2O2-induced mitophagy. Moreover, the inhibition of Akt attenuated the protective effect of astaxanthin against H2O2-induced cytotoxicity. Taken together, astaxanthin might inhibit H2O2-induced apoptosis by protecting mitochondrial function and reducing mitophagy. The results also indicate that the Akt/mTOR signaling pathway was critical for the protection of astaxanthin against H2O2-induced cytotoxicity. The results from the present study suggest that astaxanthin can reduce neuronal oxidative injury and may have the potential to be used for preventing neurotoxicity associated with neurodegenerative diseases.

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Section: Effects Of Astaxanthin On Cell Survival Mitochondrial Functi...mentioning

confidence: 99%

Section: Effects Of Astaxanthin On Cell Survival Mitochondrial Functi...mentioning

confidence: 99%

Astaxanthin Inhibits H2O2-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR Activation

Yan,

Ding,

Zhang

et al. 2024

Marine Drugs

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“…However, it faces limitations, including potential biases in data collection and the challenge of generalizing findings to other regions. Recommendations for future research include a focus on improving prenatal and perinatal care, especially in high-risk areas, and exploring strategies for early detection and intervention in cases of neonatal hypoxia (14,15,23).…”

Section: Discussionmentioning

confidence: 99%

“…This region, characterized by its high mountain ranges, streams, lakes, and numerous villages, is geographically delineated by several mountain ranges which separate it from neighboring districts. Historically part of the Swat Valley, District Buner is now an independent district, situated approximately 120 kilometers from the city of Peshawar (14,15). Data for this study were gathered using a direct questionnaire method.…”

Section: Methodsmentioning

confidence: 99%

Prevalence of Neonatal Hypoxia in District Buner, Pakistan

Khan,

Asif,

Razaq

et al. 2024

JHRR

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Background: Neonatal hypoxia, or hypoxic ischemic encephalopathy (HIE), is a significant cause of neonatal morbidity and mortality, especially in developing countries. The condition arises from insufficient oxygen or blood flow to the neonate's brain, leading to various degrees of neurological impairment. This study aims to shed light on the prevalence and characteristics of neonatal hypoxia in District Buner, Khyber Pakhtunkhwa, Pakistan, a region where limited research has been conducted on this critical issue. Objective: The primary objective of this study was to determine the prevalence of neonatal hypoxia in District Buner and to analyse the distribution of its severity across different tehsils within the district. Methods: This retrospective study was conducted from August 2021 to August 2022. Data were collected from several government and private hospitals, including DHQ Daggar, Buner Medical Complex, and Hamdard Medical Center. A total of 753 neonatal hypoxia cases were identified and classified into three categories based on severity: mild (HIE I), moderate (HIE II), and severe (HIE III). The classification was based on Apgar scores and clinical symptoms. The data were statistically analysed using Microsoft Excel 2016 and SPSS software version 25. Results: Out of the 753 neonatal hypoxia cases, 299 (39.7%) were classified as HIE I, 276 (36.6%) as HIE II, and 132 (17.5%) as HIE III. There were 46 fatalities (6.1%) reported. The study also revealed a gender disparity, with males (402 cases, 53.4%) more frequently affected than females (351 cases, 46.6%). The highest incidence of neonatal hypoxia was observed in Tehsil Daggar (25.9%), while Tehsil Khudokhail reported the lowest (6.2%). Conclusion: The study highlights a significant prevalence of neonatal hypoxia in District Buner, with milder forms of HIE being more common. The findings underscore the need for improved obstetric and neonatal care, especially in areas with higher prevalence, to reduce neonatal morbidity and mortality associated with HIE.

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“… 170 In addition, similar effects have been reported in animal and cell models of cerebral I/R that were treated with ginkgolide B derivative XQ-1H by gavage 180 and oxymatrine via intraperitoneal injection. 188 …”

Section: Wnt Pathways and Organ I/r Injurymentioning

confidence: 99%

Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets

Zhang,

Liu,

Meng

et al. 2024

Sig Transduct Target Ther

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Ischemia-reperfusion (I/R) injury paradoxically occurs during reperfusion following ischemia, exacerbating the initial tissue damage. The limited understanding of the intricate mechanisms underlying I/R injury hinders the development of effective therapeutic interventions. The Wnt signaling pathway exhibits extensive crosstalk with various other pathways, forming a network system of signaling pathways involved in I/R injury. This review article elucidates the underlying mechanisms involved in Wnt signaling, as well as the complex interplay between Wnt and other pathways, including Notch, phosphatidylinositol 3-kinase/protein kinase B, transforming growth factor-β, nuclear factor kappa, bone morphogenetic protein, N-methyl-D-aspartic acid receptor-Ca2+-Activin A, Hippo-Yes-associated protein, toll-like receptor 4/toll-interleukine-1 receptor domain-containing adapter-inducing interferon-β, and hepatocyte growth factor/mesenchymal-epithelial transition factor. In particular, we delve into their respective contributions to key pathological processes, including apoptosis, the inflammatory response, oxidative stress, extracellular matrix remodeling, angiogenesis, cell hypertrophy, fibrosis, ferroptosis, neurogenesis, and blood-brain barrier damage during I/R injury. Our comprehensive analysis of the mechanisms involved in Wnt signaling during I/R reveals that activation of the canonical Wnt pathway promotes organ recovery, while activation of the non-canonical Wnt pathways exacerbates injury. Moreover, we explore novel therapeutic approaches based on these mechanistic findings, incorporating evidence from animal experiments, current standards, and clinical trials. The objective of this review is to provide deeper insights into the roles of Wnt and its crosstalk signaling pathways in I/R-mediated processes and organ dysfunction, to facilitate the development of innovative therapeutic agents for I/R injury.

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Neuroprotective effects of oxymatrine on hypoxic–ischemic brain damage in neonatal rats by activating the Wnt/β-catenin pathway

Cited by 9 publications

References 53 publications

Astaxanthin Inhibits H2O2-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR Activation

Astaxanthin Inhibits H2O2-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR Activation

Prevalence of Neonatal Hypoxia in District Buner, Pakistan

Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets

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