Effects of inhibition of miR-155-5p in neural stem cell subarachnoid transplant on rats with cerebral infarction

Wang, Dong; Wang, Liang; Bai, Lin; Du, Yuanyuan; Liu, Luji; Chen, Xiang

doi:10.1089/hum.2019.118

Cited by 2 publications

(3 citation statements)

References 19 publications

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“…Cerebral infarction, a clinically common cerebrovascular disease, usually occurs in elderly patients and leads to nervous system damage, including motor and sensory dysfunctions of limbs, thereby triggering neurological deficits and resulting in the death of patients in severe cases. Therefore, it is a ubiquitous critical disease in clinic (12,13). It is essential to effectively treat cerebral infarction, accelerate the rehabilitation of nervous system injury and neurological deficits following cerebral infarction and relieve the limb motor dysfunction, sensory disturbance and speech disorder, thereby significantly improving the quality of life of patients with cerebral infarction and reducing the economic burdens on their family and society.…”

Section: Discussionmentioning

confidence: 99%

Butylphthalide inhibits nerve cell apoptosis in cerebral infarction rats via the JNK/p38 MAPK signaling pathway

Xia

Wang

et al. 2021

Exp Ther Med

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The aim of the present study was to investigate the influence of butylphthalide on nerve cell apoptosis in rats with cerebral infarction through the c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) signaling pathway. A total of 36 Sprague-Dawley rats were randomly divided into sham-operation group (n=12), model group (n=12) and butylphthalide group (n=12). Additionally, qPCR was performed to measure the mRNA expression of Bax and Bcl-2, and a TUNEL assay was conducted to investigate the cell apoptosis. Compared with the sham-operation group, the model group and the butylphthalide group had notably increased Zea-Longa scores (P<0.05), while the butylphthalide group exhibited a markedly decreased Zea-Longa score, compared with the model group (P<0.05). The positive expression of Bax was markedly higher (P<0.05), while that of Bcl-2 was notably lower in the model group and the butylphthalide group (P<0.05), compared with those in the sham-operation group. Furthermore, the positive expression of Bax was notably decreased (P<0.05), while that of Bcl-2 was markedly increased in the butylphthalide group in comparison with those in model group (P<0.05). The model group and the butylphthalide group had markedly higher relative protein expression levels of p-JNK and p-p38 MAPK than the sham-operation group (P<0.05), and the butylphthalide group displayed notably lower relative protein expression levels of p-JNK and p-p38 MAPK than the model group (P<0.05).The relative mRNA expression level of Bax was markedly increased (P<0.05), while that of Bcl-2 was notably decreased in the model group and the butylphthalide group (P<0.05), compared with those in the sham-operation group. Compared with those in the model group, the relative mRNA expression level of Bax decreased markedly (P<0.05), and that of Bcl-2 increased notably in the butylphthalide group (P<0.05). The apoptotic rate was markedly higher in the model group and the butylphthalide group than that in the sham-operation group (P<0.05), but it was notably lower in the butylphthalide group than that in the model group (P<0.05). In conclusion, butylphthalide may inhibit nerve cell apoptosis in rats with cerebral infarction to exert a protective effect, which may be associated with the JNK/p38 MAPK signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Butylphthalide inhibits nerve cell apoptosis in cerebral infarction rats via the JNK/p38 MAPK signaling pathway

Xia

Wang

et al. 2021

Exp Ther Med

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“…By contrast, downregulation of miRNA-210 expression markedly inhibits the gene and protein expression of HIF-1α and VEGF (83). The expression levels of miR-376b-5p, miR-433, miR-335 and miR-155-5p are negatively associated with the expression levels of HIF-1α (84)(85)(86)(87). miR-376b-5p inhibits angiogenesis after cerebral ischemia via the HIF-1α-mediated VEGFA-Notch1 signaling pathway (84).…”

Section: Hif-1α Protects the Brain Via The Regulation Of Endogenous Substancesmentioning

confidence: 99%

“…miR-335 regulates HIF-1α expression and also affects neurovascular permeability, cell death and the blood-brain barrier, resulting in a reduction in infarct volume (86). Furthermore, a recent study has demonstrated that miR-155-5p targets HIF-1α in NSCs (87). Inhibition of miR-155-5p may promote the viability of NSCs and inhibit cell apoptosis induced by oesophago-gastro-duodenoscopy (OGD).…”

Section: Hif-1α Protects the Brain Via The Regulation Of Endogenous Substancesmentioning

confidence: 99%

HIF‑1α in cerebral ischemia (Review)

Dong

Han

2021

Mol Med Rep

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Cerebral ischemic injury may lead to a series of serious brain diseases, death or different degrees of disability. Hypoxia-inducible factor-1α (HIF-1α) is an oxygen-sensitive transcription factor, which mediates the adaptive metabolic response to hypoxia and serves a key role in cerebral ischemia. HIF-1α is the main molecule that responds to hypoxia. HIF-1α serves an important role in the development of cerebral ischemia by participating in numerous processes, including metabolism, proliferation and angiogenesis. The present review focuses on the endogenous protective mechanism of cerebral ischemia and elaborates on the role of HIF-1α in cerebral ischemia. In addition, it focuses on cerebral ischemia interventions that act on the HIF-1α target, including biological factors, non-coding RNA, hypoxic-ischemic preconditioning and drugs, and expands upon the measures to strengthen the endogenous compensatory response to support HIF-1α as a therapeutic target, thus providing novel suggestions for the treatment of cerebral ischemia. Contents1. Introduction 2. Literature screening method 3. Role of HIF-1α in cerebral ischemia 4. HIF-1α protects the brain via the regulation of endogenous substances 5. Role of HIF-1α in cerebral ischemic preconditioning (IPC) 6. Role of HIF-1α in the protective effects of natural compounds against cerebral ischemia 7. Concluding remarks and future perspectives

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Effects of inhibition of miR-155-5p in neural stem cell subarachnoid transplant on rats with cerebral infarction

Cited by 2 publications

References 19 publications

Butylphthalide inhibits nerve cell apoptosis in cerebral infarction rats via the JNK/p38 MAPK signaling pathway

Butylphthalide inhibits nerve cell apoptosis in cerebral infarction rats via the JNK/p38 MAPK signaling pathway

HIF‑1α in cerebral ischemia (Review)

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