Decorin alleviated chronic hydrocephalus via inhibiting TGF-β1/Smad/CTGF pathway after subarachnoid hemorrhage in rats

Yan, Hui; Chen, Yujie; Li, Lingyong; Jiang, Jiaode; Wu, Guangyong; Zuo, Yuchun; Zhang, Junyi; Feng, Hua; Yan, Xiao‐Xin; Liu, Fei

doi:10.1016/j.brainres.2015.11.004

Cited by 47 publications

(46 citation statements)

References 47 publications

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“…Beside the proliferation of leptomeningeal cells (Figure 1), studies at present primarily target the pathological obstruction of AGs, including the mechanical blockage and fibrosis of AGs (Figure 2). Researchers have been long working on attenuating this pathogenesis to deal with HCP [6, 7]. …”

Section: Etiologymentioning

confidence: 99%

“…Along with the gradual disclosure of mechanisms in HCP in recent years, some experimental agents are found to be potentially effective in improving the outcomes of patients [7, 39]. Minocycline is reported to be effective in reducing the gliosis and delaying the development of HCP in rat model [40].…”

Section: Treatmentmentioning

confidence: 99%

“…Minocycline is reported to be effective in reducing the gliosis and delaying the development of HCP in rat model [40]. And decorin may be beneficial for the long-term of HCP [7]. On the other hand, in neonatal rats with germinal matrix hemorrhage, deferoxamine attenuates long-term complications including posthemorrhagic dilation of ventricles [41].…”

Section: Treatmentmentioning

confidence: 99%

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Hydrocephalus after Subarachnoid Hemorrhage: Pathophysiology, Diagnosis, and Treatment

Chen

Luo

Reis

et al. 2017

BioMed Research International

123

131

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Hydrocephalus (HCP) is a common complication in patients with subarachnoid hemorrhage. In this review, we summarize the advanced research on HCP and discuss the understanding of the molecular originators of HCP and the development of diagnoses and remedies of HCP after SAH. It has been reported that inflammation, apoptosis, autophagy, and oxidative stress are the important causes of HCP, and well-known molecules including transforming growth factor, matrix metalloproteinases, and iron terminally lead to fibrosis and blockage of HCP. Potential medicines for HCP are still in preclinical status, and surgery is the most prevalent and efficient therapy, despite respective risks of different surgical methods, including lamina terminalis fenestration, ventricle-peritoneal shunting, and lumbar-peritoneal shunting. HCP remains an ailment that cannot be ignored and even with various solutions the medical community is still trying to understand and settle why and how it develops and accordingly improve the prognosis of these patients with HCP.

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Section: Etiologymentioning

confidence: 99%

Section: Treatmentmentioning

confidence: 99%

Section: Treatmentmentioning

confidence: 99%

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Hydrocephalus after Subarachnoid Hemorrhage: Pathophysiology, Diagnosis, and Treatment

Chen

Luo

Reis

et al. 2017

BioMed Research International

123

131

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show abstract

“…After delivery, pups were euthanized with over dose isoflurane. Cerebrospinal fluid (CSF) from fetal brain was collected via the cisterna magna puncture as described previously and stored at −70 °C until further analysis (Yan et al, 2016). Fetal brain tissues were dissected for mRNA and protein analysis.…”

Section: Methodsmentioning

confidence: 99%

“…Western blot analysis was performed to determine indicated protein levels in the fetal brain according to a previous procedure (Yan et al, 2016). Brain tissues were homogenized in lysis buffer supplemented with protease and phosphatase inhibitors.…”

Section: Western Blot Analysismentioning

confidence: 99%

Protective effects of quercetin against brain injury in a rat model of lipopolysaccharide‐induced fetal brain injury

Wang

Liu

2018

Intl J of Devlp Neuroscience

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Maternal exposure to lipopolysaccharide (LPS), a bacterial endotoxin produced during infection, leads to disruption in fetal brain development and causes newborn brain injury. Quercetin (QR) is a multipotent flavonoid that functions as an antioxidant and protects against inflammation and neurodegeneration. In this study, we explored the potential functions of QR in alleviating maternal LPS exposure induced fetal brain damage. Pregnant rats at late gestational stages were treated with saline, LPS, QR, LPS and QR. Brain injury biomarker TGF‐1β was assessed in cerebrospinal fluid (CSF) and brain tissue of newborn rats. Pro‐inflammatory cytokines, apoptosis markers and oxidative stress indicators were evaluated. We found that LPS treatment induced an increased production of TGF‐1β which was suppressed by QR administration. LPS enhanced pro‐apoptotic Bax and inhibited anti‐apoptotic Bcl‐2 expression. QR reduced that ratio of Bax and Bcl‐2 that was high in LPS treated brain tissue. Additionally, QR suppressed oxidative stress induced by LPS. Finally, QR reduced the levels of pro‐inflammatory cytokines that were produced as a result of LPS exposure. In summary, our study indicates that QR potently alleviates maternal LPS exposure induced fetal brain injury in rats, making it a potential therapeutic for suppressing infant brain damage as a result of maternal infection.

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Hydrocephalus Following Aneurysmal Subarachnoid Hemorrhage

DornbosIII

Smith

Shah

et al. 2018

Cerebrospinal Fluid Disorders

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Decorin alleviated chronic hydrocephalus via inhibiting TGF-β1/Smad/CTGF pathway after subarachnoid hemorrhage in rats

Cited by 47 publications

References 47 publications

Hydrocephalus after Subarachnoid Hemorrhage: Pathophysiology, Diagnosis, and Treatment

Hydrocephalus after Subarachnoid Hemorrhage: Pathophysiology, Diagnosis, and Treatment

Protective effects of quercetin against brain injury in a rat model of lipopolysaccharide‐induced fetal brain injury

Hydrocephalus Following Aneurysmal Subarachnoid Hemorrhage

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