Peroxisome Proliferator-Activated Receptor γ Agonist Rosiglitazone Protects Blood–Brain Barrier Integrity Following Diffuse Axonal Injury by Decreasing the Levels of Inflammatory Mediators Through a Caveolin-1-Dependent Pathway

Zhao, Yonglin; Wei, Xing; Song, Jin‐Ning; Zhang, Ming; Huang, Tingqin; Qin, Jie

doi:10.1007/s10753-018-0940-2

Cited by 24 publications

(29 citation statements)

References 38 publications

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“…A very recent study found that rosiglatizone can protect BBB by attenuating inflammation through a CAV1-depedent pathway. It is yet to be studied in the state of diabetes [221].…”

Section: Future Perspectivesmentioning

confidence: 99%

Role of Caveolin-1 in Diabetes and Its Complications

Haddad

Madhoun

Nizam

et al. 2020

Oxidative Medicine and Cellular Longevity

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It is estimated that in 2017 there were 451 million people with diabetes worldwide. These figures are expected to increase to 693 million by 2045; thus, innovative preventative programs and treatments are a necessity to fight this escalating pandemic disorder. Caveolin-1 (CAV1), an integral membrane protein, is the principal component of caveolae in membranes and is involved in multiple cellular functions such as endocytosis, cholesterol homeostasis, signal transduction, and mechanoprotection. Previous studies demonstrated that CAV1 is critical for insulin receptor-mediated signaling, insulin secretion, and potentially the development of insulin resistance. Here, we summarize the recent progress on the role of CAV1 in diabetes and diabetic complications.

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“…A very recent study found that rosiglatizone can protect BBB by attenuating inflammation through a CAV1-depedent pathway. It is yet to be studied in the state of diabetes [221].…”

Section: Future Perspectivesmentioning

confidence: 99%

Role of Caveolin-1 in Diabetes and Its Complications

Haddad

Madhoun

Nizam

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Studies have shown that RSG can increase the expression of caveolin-1 in cancer cells and macrophages [28,29]. Recently, Zhao et al provided evidence that RSG can protect brain tissue and BBB by increasing the level of caveolin-1 in diffuse axonal injury [10,11]. However, whether RSG can play a protective role on BBB in animal models of cerebral ischemia/reperfusion injury via a caveolin-1dependent pathway remains unknown, so we conducted this experiment.…”

Section: Discussionmentioning

confidence: 98%

Rosiglitazone Protects Blood-Brain Barrier Integrity Following Ischemic Stroke by Reducing MMP-9 Expression Through a Caveolin-1-Dependent Pathway.

Huang

Zhong

et al. 2020

Preprint

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Background: Rosiglitazone (RSG) is a widely used antidiabetic drug which activates peroxisome proliferator-activated receptor-γ. Recent work have shown that RSG can up-regulate caveolin-1 levels and ameliorate both chronic and acute brain injury. However, whether rosiglitazone can ameliorate ischemic injury in the brain via a caveolin-1-dependent pathway remains unknown. Methods: Adult male sprague-dawley rats were randomly divided into sham operation group, model group, rosiglitazone group and rosiglitazone+daidzein group. The rat models of middle cerebral artery occlusion (MCAO) was established using the suture method, with ischemia for 2 hours and reperfusion for 22 hours. Neurological deficits were evaluated by the methods of Longa’s standard scoring. Cerebral infarction volume was observed by staining with 2, 3, 5-triphenyltetrazolium chloride. Evans blue content reflects BBB permeability. The expressions of caveolin-1, matrix metalloproteinase-9(MMP-9) and occludin were detected by immunofluorescent staining and western blot. Results: In this study, we found that the expression of caveolin-1 was increased in a rat model of stroke, and treatment with RSG significantly increased the levels of caveolin-1, reduced the release of MMP-9, and increased the expression of occludin. On the other hand, a caveolin-1 inhibitor daidzein canceled the protective roles of RSG in the MCAO model. Conclusions: These data unveil that RSG might protect blood-brain barrier integrity by down-regulating the levels of MMP-9 via a caveolin-1-dependent pathway.

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“…Studies have shown that RSG can increase the expression of caveolin-1 in cancer cells and macrophages [27,28]. Recently, Zhao et al provided evidence that RSG can protect brain tissue and BBB by increasing the level of caveolin-1 in diffuse axonal injury [10,11]. However, whether RSG can play a protective role on BBB in animal models of cerebral ischemia/reperfusion injury via a caveolin-1-dependent pathway remains unknown, so we conducted this experiment.…”

Section: Discussionmentioning

confidence: 99%

“…Administration of PPAR-γ agonists has been shown to protect against cerebral ischemia through multiple mechanisms, such as by inhibition of post-ischemic oxidative stress [5,6], apoptosis [5], and ischemia-induced in ammation [6][7][8][9]. Recent in vitro and vivo research, Rosiglitazone (RSG), a PPARγ agonist, was shown to increase caveolin-1 expression and protect against traumatic brain injury [10,11]. Caveolin-1 is a principal marker of caveolae which are invaginations of the plasma membrane [12].…”

Section: Introductionmentioning

confidence: 99%

Rosiglitazone Protects Blood-Brain Barrier Integrity Following Ischemic Stroke by Reducing MMP-9 Expression Through a Caveolin-1-Dependent Pathway.

Huang

Zhong

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Rosiglitazone (RSG) is a widely used antidiabetic drug which activates peroxisome proliferator-activated receptor-γ. Recent work have shown that RSG can up-regulate caveolin-1 levels and ameliorate both chronic and acute brain injury. However, whether rosiglitazone can ameliorate ischemic injury in the brain via a caveolin-1-dependent pathway remains unknown. Methods: Adult male sprague-dawley rats were randomly divided into sham operation group, model group, rosiglitazone group and rosiglitazone+daidzein group. The rat models of middle cerebral artery occlusion (MCAO) was established using the suture method, with ischemia for 2 hours and reperfusion for 22 hours. Neurological deficits were evaluated by the methods of Longa’s standard scoring. Cerebral infarction volume was observed by staining with 2, 3, 5-triphenyltetrazolium chloride. Evans blue content reflects BBB permeability. The expressions of caveolin-1, matrix metalloproteinase-9(MMP-9) and occludin were detected by immunofluorescent staining and western blot. Results: In this study, we found that the expression of caveolin-1 was increased in a rat model of stroke, and treatment with RSG significantly increased the levels of caveolin-1, reduced the release of MMP-9, and increased the expression of occludin. On the other hand, a caveolin-1 inhibitor daidzein canceled the protective roles of RSG in the MCAO model.Conclusions: These data unveil that RSG might protect blood-brain barrier integrity by down-regulating the levels of MMP-9 via a caveolin-1-dependent pathway.

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Peroxisome Proliferator-Activated Receptor γ Agonist Rosiglitazone Protects Blood–Brain Barrier Integrity Following Diffuse Axonal Injury by Decreasing the Levels of Inflammatory Mediators Through a Caveolin-1-Dependent Pathway

Cited by 24 publications

References 38 publications

Role of Caveolin-1 in Diabetes and Its Complications

Role of Caveolin-1 in Diabetes and Its Complications

Rosiglitazone Protects Blood-Brain Barrier Integrity Following Ischemic Stroke by Reducing MMP-9 Expression Through a Caveolin-1-Dependent Pathway.

Rosiglitazone Protects Blood-Brain Barrier Integrity Following Ischemic Stroke by Reducing MMP-9 Expression Through a Caveolin-1-Dependent Pathway.

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