Acupuncture Ameliorates Neuronal Cell Death, Inflammation, and Ferroptosis and Downregulated miR-23a-3p After Intracerebral Hemorrhage in Rats

Kong, Ying; Li, Shulin; Zhang, Miao; Xu, Wenting; Chen, Qiuxin; Zheng, Lihong; Liu, Peng; Zou, Wei

doi:10.1007/s12031-020-01770-x

Cited by 32 publications

(22 citation statements)

References 59 publications

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“…Further study found that SA could reduce inflammatory injury and brain edema by regulating the Mincle/Syk pathway (Liu et al, 2018b). SA could reduce neuronal death and inflammation and alleviate brain edema after intracerebral hemorrhage by downregulating miR-23a-3p (Kong et al, 2021). Research has confirmed that acupuncture may enhance mitochondrial respiratory chain enzyme activity and improve mitochondrial dysfunction (Zhang et al, 2014).…”

Section: Discussionmentioning

confidence: 95%

Scalp Acupuncture Attenuates Brain Damage After Intracerebral Hemorrhage Through Enhanced Mitophagy and Reduced Apoptosis in Rats

Liu

Dai

et al. 2021

Front. Aging Neurosci.

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To study the effect of scalp acupuncture (SA) on the mitophagy signaling pathway in the caudate nucleus of Sprague-Dawley rats following intracerebral hemorrhage (ICH). An ICH model was established by injecting autologous arterial blood into the caudate nucleus in 200 male Sprague-Dawley rats, which were divided into five groups: sham, ICH, 3-methyladenine group (3-MA, 30 mg/kg), SA, and SA+3-MA. Animals were analyzed at 6 and 24 h as well as at 3 and 7 days. Composite neurological scale score was significantly higher in the SA group than in the ICH group. Transmission electron microscopy showed less structural damage and more autophagic vacuoles within brain in the SA group than in the ICH group. SA group showed higher levels of Beclin1, Parkin, PINK1, NIX protein, and a lower level of Caspase-9 in brain tissue. These animals consequently showed less neural cell apoptosis. Compared with the SA group, however, the neural function score and levels of mitophagy protein in the SA+3-MA group were decreased, neural cell apoptosis was increased with more severe structural damage, which suggested that 3-MA may antagonize the protective effect of SA on brain in rats with ICH. SA may mitigate the neurologic impairment after ICH by enhancing mitophagy and reducing apoptosis.

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Section: Discussionmentioning

confidence: 95%

Scalp Acupuncture Attenuates Brain Damage After Intracerebral Hemorrhage Through Enhanced Mitophagy and Reduced Apoptosis in Rats

Liu

Dai

et al. 2021

Front. Aging Neurosci.

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“…miR-23a-3p regulates cell proliferation and metastasis through inhibition of PTEN [ 103 ], a regulator of Nrf2 [ 104 ]. Notably, in a rat blood-injection model of ICH, the expression of miR-23a-3p was increased in the perihematomal brain region 3 days after ICH [ 105 ], implicating its possible role in the pathophysiology of ICH. Consistently, the genetic inhibition of miR-23a-3p attenuated ICH-induced neurodegeneration, ferroptosis (an iron-dependent cell death), and the release of proinflammatory cytokines in rats [ 105 ].…”

Section: Microrna and Ich-induced Neuroinflammationmentioning

confidence: 99%

“…Notably, in a rat blood-injection model of ICH, the expression of miR-23a-3p was increased in the perihematomal brain region 3 days after ICH [ 105 ], implicating its possible role in the pathophysiology of ICH. Consistently, the genetic inhibition of miR-23a-3p attenuated ICH-induced neurodegeneration, ferroptosis (an iron-dependent cell death), and the release of proinflammatory cytokines in rats [ 105 ]. Of note, miR-23a-3p antagomir-mediated neuroprotection after ICH was associated with an induction of HO-1, a critical downstream target of Nrf2 [ 106 ].…”

Section: Microrna and Ich-induced Neuroinflammationmentioning

confidence: 99%

“…Taken together, miR dysfunction after ICH contributes to microglial polarization and cytokine release, critical brain responses that play roles in secondary brain damage and brain recovery. Besides neuroinflammation, miR-23a-3p [ 105 ] and miR-183-5p [ 164 ] may also regulate oxidative brain damage, further implicating the potential of targeting miR in improving neurological outcomes after ICH.…”

Section: Therapeutic and Diagnostic Implications Of Micrornamentioning

confidence: 99%

“…Additionally, the members in the same family of miR may exert different functional roles. To this end, miR-23a-3p has a neurodegenerative role [ 105 ], while miR-23b has a neuroprotective role after ICH [ 111 ]. Although they are both derived from the same double-stranded precursor, they may have different functional targets.…”

Section: Therapeutic and Diagnostic Implications Of Micrornamentioning

confidence: 99%

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Dysregulation of microRNA and Intracerebral Hemorrhage: Roles in Neuroinflammation

Kashif

Shah

Sukumari‐Ramesh

2021

IJMS

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Intracerebral hemorrhage (ICH) is a major public health problem and devastating subtype of stroke with high morbidity and mortality. Notably, there is no effective treatment for ICH. Neuroinflammation, a pathological hallmark of ICH, contributes to both brain injury and repair and hence, it is regarded as a potential target for therapeutic intervention. Recent studies document that microRNAs, small non-coding RNA molecules, can regulate inflammatory brain response after ICH and are viable molecular targets to alter brain function. Therefore, there is an escalating interest in studying the role of microRNAs in the pathophysiology of ICH. Herein, we provide, for the first time, an overview of the microRNAs that play roles in ICH-induced neuroinflammation and identify the critical knowledge gap in the field, as it would help design future studies.

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Photothermal Microneedle Hydrogel Patch for Refractory Soft Tissue Injuries through Thermosensitized Anti‐Inflammaging Modulation

Zhu,

Liu,

Zhang

et al. 2024

Small Structures

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Soft tissue injuries (STIs) are the most common cause of extremity pain and motion dysfunction. Persistent inflammatory activation of immune cells characterized by senescence‐associated secretory phenotype (SASP) and mitochondrial stress are considered the primary causes of STIs, a pathological process also termed inflammaging. Meanwhile, scavenging excessive “cellular waste” in the inflammaging microenvironment and further activating tissue repair processes remain elusive. Herein, an anti‐inflammaging photothermal hydrogel microneedle patch for treating STIs is developed. Taurine‐loaded Prussian blue nanoparticles (Taurine@PB) are encapsulated in a methacrylate‐based hyaluronic acid hydrogel (HAMA) and further fabricated into taurine@PB@HAMA@microneedles (TPH@MN) patches. The acidic microenvironment of chronic inflammation and mild photothermal effects promote taurine release and anti‐inflammaging immunomodulation, inhibiting mitochondrial stress via the SIRT3‐NF‐κB axis to promote glycolytic metabolic microenvironment of neutrophils reprogramming toward oxidative phosphorylation metabolism. Furthermore, TPH@MN activates macrophage efferocytosis and initiates the process of tissue repair. In mouse models of chronic diabetic wounds and tibialis anterior (TA) muscle injury, TPH@MN inhibits SASP expression and promotes STIs healing through thermosensitized anti‐inflammaging immunomodulation. In summary, TPH@MN circumvents the side effects of systemic administration, providing new translatable options in the treatment modalities for patients suffering from STIs worldwide.

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Acupuncture Ameliorates Neuronal Cell Death, Inflammation, and Ferroptosis and Downregulated miR-23a-3p After Intracerebral Hemorrhage in Rats

Cited by 32 publications

References 59 publications

Scalp Acupuncture Attenuates Brain Damage After Intracerebral Hemorrhage Through Enhanced Mitophagy and Reduced Apoptosis in Rats

Scalp Acupuncture Attenuates Brain Damage After Intracerebral Hemorrhage Through Enhanced Mitophagy and Reduced Apoptosis in Rats

Dysregulation of microRNA and Intracerebral Hemorrhage: Roles in Neuroinflammation

Photothermal Microneedle Hydrogel Patch for Refractory Soft Tissue Injuries through Thermosensitized Anti‐Inflammaging Modulation

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