Hydroxysafflor yellow A protects methylglyoxal-induced injury in the cultured human brain microvascular endothelial cells

Li, Wenlu; Liu, Jie; He, Ping; Ni, Zhenzhen; Hu, Yangmin; Xu, Huimin; Dai, Haibin

doi:10.1016/j.neulet.2013.06.007

Cited by 32 publications

(26 citation statements)

References 30 publications

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“…The ability of HSYA to increase Ang 1 expression may be a mechanism by which HSYA protects cells from the effects of various injuries, such as ischemia [35,47], hypoxia [18,24], and methylglyoxal exposure [48], by inhibiting apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Hydroxysafflor Yellow A Promotes Angiogenesis via the Angiopoietin 1/ Tie-2 Signaling Pathway

Chen¹,

Chen

Pang

et al. 2016

J Vasc Res

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Background: The flowers of Carthamus tinctorius L. are widely used in traditional Chinese medicine to treat cerebrovascular and cardiovascular diseases. Hydroxysafflor yellow A (HSYA), the main constituent of C. tinctorius L. flowers, is known for its multiple biological activities. The present study investigated the effects of HSYA on angiogenesis in vitro and in a mouse hindlimb ischemia model. Methods: Using human umbilical vein endothelial cells (HUVEC) in vitro and a mouse hindlimb ischemia model in vivo, the angiogenic role of HSYA was evaluated. Results: HSYA significantly increased the capillary-like tube formation and migration of HUVEC. HSYA not only induced a rise in the expression of angiopoietin 1 and Tie-2 but it also increased phosphorylation of Tie-2, Akt, and extracellular signal-regulated kinase 1/2. Furthermore, an anti-Tie-2 neutralizing antibody significantly inhibited HSYA-induced HUVEC tube formation and migration. In vivo, the recovery of perfusion of ischemic hindlimb tissue after femoral artery interruption was significantly increased in HSYA-treated mice compared to vehicle controls. Consistent with these results, the arteriole and capillary densities in ischemic gastrocnemius muscles were significantly increased in HSYA-treated mice. Conclusions: These results indicate the potential utility of HSYA for the treatment of ischemic diseases.

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Section: Discussionmentioning

confidence: 99%

Hydroxysafflor Yellow A Promotes Angiogenesis via the Angiopoietin 1/ Tie-2 Signaling Pathway

Chen¹,

Chen

Pang

et al. 2016

J Vasc Res

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“…Brain edema, traditionally classified as vasogenic and cytotoxic edema, serves a critical role in cerebral I/R injury (1,2,7). Cytotoxic edema occurs due to increased water permeability of cell membranes, which is associated with the aquaporin family, a group of selective water transport membrane proteins (8,9).…”

Section: Introductionmentioning

confidence: 99%

Resveratrol ameliorates oxidative stress and inhibits aquaporin 4 expression following rat cerebral ischemia-reperfusion injury

Tan

Liu

et al. 2015

Molecular Medicine Reports

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Abstract. Cerebral ischemia-reperfusion (I/R) is associated with increased levels of reactive oxygen species (ROS) and brain edema, which lead to the deterioration of patient prognosis. Resveratrol serves a neuroprotective role in I/R injury, and this role may be associated with its anti-oxidative effects. However, resveratrol's mechanism of action in cerebral I/R injury remains to be fully understood. In order to investigate the effect of resveratrol in cerebral I/R-induced injury, male Sprague-Dawley rats were randomly assigned to four groups: The sham-operation group, the I/R group and the edaravone and resveratrol groups (I/R + E and I/R + R groups). Infarct volume was evaluated by 2,3,5-tripenyltetrazolium chloride staining, brain edema was evaluated by the water content in the reperfused brain and malondialdehyde (MDA) was measured by the thiobarbituric acid method. Superoxide dismutase (SOD) levels were measured using the Total Superoxide Dismutase Assay kit. Inducible nitric oxide synthase (iNOS) levels in the hippocampus and cortex were measured by ELISA, and aquaporin 4 (AQP4) expression was measured by immunohistochemical staining and western blot analysis. The results demonstrated that resveratrol reduced the infarct volume and the incidence of brain edema and reduced neurological deficits. These outcomes were accompanied by reduced levels of MDA, iNOS and AQP4, and increased SOD levels in cerebral I/R injury. In conclusion, resveratrol protected against cerebral I/R injury by ameliorating oxidative stress and reducing AQP4 expression.

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“…Impedance data reflecting changes in cell adhesion, shape and number were confirmed by MTT tests measuring the metabolic activity of cells. Our data lend support to and expand previous findings on the effect of methylglyoxal on human brain endothelial cells Li et al, 2013a;Li et al, 2013b;Li et al, 2013c). We selected the human hCMEC/D3 cell line as a simplified model of the BBB.…”

Section: Methylglyoxal Induced Changes In Brain Endothelial Cellssupporting

confidence: 86%

Protection of the blood-brain barrier under pathological conditions

Andrea

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Hydroxysafflor yellow A protects methylglyoxal-induced injury in the cultured human brain microvascular endothelial cells

Cited by 32 publications

References 30 publications

Hydroxysafflor Yellow A Promotes Angiogenesis via the Angiopoietin 1/ Tie-2 Signaling Pathway

Hydroxysafflor Yellow A Promotes Angiogenesis via the Angiopoietin 1/ Tie-2 Signaling Pathway

Resveratrol ameliorates oxidative stress and inhibits aquaporin 4 expression following rat cerebral ischemia-reperfusion injury

Protection of the blood-brain barrier under pathological conditions

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