RNA interference-mediated silencing of S100B improves nerve function recovery and inhibits hippocampal cell apoptosis in rat models of ischemic stroke

Abstract Stroke remains a deadly and disabling disease with limited treatment tragedies due to the limitations of available treatments; novel therapies for stroke are needed. In this article, the synergistic results of dual bone marrow mesenchymal stem cells (BMSC) and fasudil treatment in rat models of ischemic stroke still requires further identification. Sprague-Dawley rats were used to construct the middle cerebral artery, occlusion models. BMSCs were incubated with fasudil, and MTT was performed to evaluate cell proliferation. The rats were treated with fasudil+BMSC, BMSC, fasudil, and saline. Blood samples were collected for complete blood count analysis and measurement of serum TNF-α levels. The neurological functions were evaluated. After the rats were sacrificed, immunohistochemical staining and TTC staining was performed. Fasudil promoted the proliferation of BMSCs and induced their differentiation into neuron-like cells. BMSCs increased the proportion of neutrophils; nevertheless, fasudil counteracted the neutrophil increase. The TUJ-1/MAP2/VIII factor expression in the fasudil+BMSC group was significantly higher than that in the other groups. The number of GFAP-positive cells decreased in the fasudil+BMSC and BMSC alone groups. The infarct volume in the fasudil+BMSC and BMSC alone groups was significantly lower than in the fasudil alone and control groups.Both BMSCs and fasudil exert neurorestorative effects in rat models of cerebral ischemia. Fasudil neutralizes the pro-inflammatory effects of BMSCs, while BMSCs and fasudil together had synergistic effects promoting neurovascular remodeling and neurological function recovery in stroke. A combination of BMSCs and fasudil provides a promising method for the treatment of ischemic stroke.

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Author Correction: Microenvironment-responsive immunoregulatory electrospun fibers for promoting nerve function recovery

Nature Communications ◽

10.1038/s41467-021-23438-9 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Kun Xi ◽

Yong Gu ◽

Jincheng Tang ◽

Hao Chen ◽

Yun Xu ◽

...

Keyword(s):

Electrospun Fibers ◽

Nerve Function ◽

Function Recovery

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Long Noncoding RNA X-Inactive Specific Transcript Regulates Neuronal Cell Apoptosis in Ischemic Stroke Through miR-98/BACH1 Axis

DNA and Cell Biology ◽

10.1089/dna.2020.6354 ◽

2021 ◽

Author(s):

Suiqing Weng ◽

Sheng Wang ◽

Jingwen Jiang

Keyword(s):

Ischemic Stroke ◽

Cell Apoptosis ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Neuronal Cell ◽

Specific Transcript

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Exendin-4 improves neuron protection and functional recovery in experimental spinal cord injury in rats through regulating PCBP2 expression

10.1101/2020.11.09.373993 ◽

2020 ◽

Author(s):

Huaichao Luo ◽

Qingwei Wang ◽

Lei Wang

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Cell Apoptosis ◽

Sham Group ◽

Sham Operation ◽

Therapeutic Effects ◽

Rat Models ◽

Apoptosis Rate ◽

Cord Injury ◽

Group A

AbstractAimsIn the present research, we assessed the therapeutic effects of Exendin-4 (Ex-4) on rat models with spinal cord injury (SCI).Materials and methods36 male Sprague–Dawley rats were randomly allocated into three groups, including sham operation group, SCI group and SCI+Ex-4 group (Ex-4 treatment (10 µg/rat) after SCI, i.p.). In the SCI group, a laminectomy was performed at the T10 vertebrae, followed by weight-drop contusion of the spinal cord. In the sham group, a laminectomy was carried out without SCI contusion.Key findingsOur results showed that Basso-Beattie-Bresnahan scale scores were significantly decreased after SCI, and were obviously improved in SCI rats with Ex-4 administration. Additionally, the water content of spinal cord in SCI group was dramatically increased than that in sham group, and after Ex-4 treatment, degree of edema of spinal cord was remarkably reduced. And also, concentration levels of inflammatory cytokines (IL-1α, IL-1β, IL-6 and TNF-α) in the spinal cord were significantly elevated after SCI, and were remarkably reduced in SCI rats with Ex-4 administration. Subsequently, cell apoptosis rate in the injured spinal cord was significantly increased, and after Ex-4 treatment, cell apoptosis rate was remarkably decreased. We also revealed that levels of PCBP2 mRNA and protein were significantly up-regulated after SCI, and were dramatically dropped in SCI rats with Ex-4 administration.SignificanceTake altogether, our findings disclosed that Ex-4 plays a role in promoting neurological function recovery and inhibiting neuronal apoptosis through effecting PCBP2 expression in SCI rat models.

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Hollow Prussian Blue Nanozymes Drive Neuroprotection against Ischemic Stroke via Attenuating Oxidative Stress, Counteracting Inflammation, and Suppressing Cell Apoptosis

Nano Letters ◽

10.1021/acs.nanolett.8b04729 ◽

2019 ◽

Vol 19 (5) ◽

pp. 2812-2823 ◽

Cited By ~ 31

Author(s):

Kai Zhang ◽

Mengjiao Tu ◽

Wei Gao ◽

Xiaojun Cai ◽

Fahuan Song ◽

...

Keyword(s):

Oxidative Stress ◽

Ischemic Stroke ◽

Prussian Blue ◽

Cell Apoptosis

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BMS-986020, a Specific LPA1 Antagonist, Provides Neuroprotection against Ischemic Stroke in Mice

Antioxidants ◽

10.3390/antiox9111097 ◽

2020 ◽

Vol 9 (11) ◽

pp. 1097

Author(s):

Bhakta Prasad Gaire ◽

Arjun Sapkota ◽

Ji Woong Choi

Keyword(s):

Ischemic Stroke ◽

Survival Rate ◽

Cell Apoptosis ◽

Functional Disability ◽

Brain Infarction ◽

Tissue Loss ◽

Neurological Deficits ◽

Neuroprotective Effects ◽

Acute Injuries

Stroke is a leading cause of death. Stroke survivors often suffer from long-term functional disability. This study demonstrated neuroprotective effects of BMS-986020 (BMS), a selective lysophosphatidic acid receptor 1 (LPA1) antagonist under clinical trials for lung fibrosis and psoriasis, against both acute and sub-acute injuries after ischemic stroke by employing a mouse model with transient middle cerebral artery occlusion (tMCAO). BMS administration immediately after reperfusion significantly attenuated acute brain injuries including brain infarction, neurological deficits, and cell apoptosis at day 1 after tMCAO. Neuroprotective effects of BMS were preserved even when administered at 3 h after reperfusion. Neuroprotection by BMS against acute injuries was associated with attenuation of microglial activation and lipid peroxidation in post-ischemic brains. Notably, repeated BMS administration daily for 14 days after tMCAO exerted long-term neuroprotection in tMCAO-challenged mice, as evidenced by significantly attenuated neurological deficits and improved survival rate. It also attenuated brain tissue loss and cell apoptosis in post-ischemic brains. Mechanistically, it significantly enhanced neurogenesis and angiogenesis in injured brains. A single administration of BMS provided similar long-term neuroprotection except survival rate. Collectively, BMS provided neuroprotection against both acute and sub-acute injuries of ischemic stroke, indicating that BMS might be an appealing therapeutic agent to treat ischemic stroke.

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