Baicalin prevents the production of hydrogen peroxide and oxidative stress induced by Aβ aggregation in SH-SY5Y cells

Yin, Fei; Liu, Jianhui; Ji, Xiuhong; Wang, Yanwen; Zidichouski, Jeffrey A.; Zhang, Junzeng

doi:10.1016/j.neulet.2011.01.055

Cited by 64 publications

(35 citation statements)

References 33 publications

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“…Furthermore, baicalin is reported to attenuate ischemic brain damage through inhibiting NF-jB p65 activation [19]. In addition, baicalin protects SH-SY5Y cells from oxidative injuries induced by Ab1-42 aggregation through decreasing H 2 O 2 production [20]. To our best knowledgement, however, it is never known that whether baicalin could improve the cerebral ischemia-induced BBB disruption.…”

Section: Discussionmentioning

confidence: 99%

Effect of Baicalin on Matrix Metalloproteinase-9 Expression and Blood–Brain Barrier Permeability Following Focal Cerebral Ischemia in Rats

Yang

Liang

et al. 2011

Neurochem Res

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Focal cerebral ischemia results in an increased expression of matrix metalloproteinase-9 (MMP-9), which induces vasogenic brain edema via disrupting the blood-brain barrier (BBB) integrity. Recent studies from our laboratory showed that baicalin reduces ischemic brain damage by inhibiting inflammatory reaction and neuronal apoptosis in a rat model of focal cerebral ischemia. In the present study, we first explored the effect of baicalin on the neuronal damage, brain edema and BBB permeability, then further investigated its potential mechanisms. Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (MCAO). Baicalin was administrated by intraperitoneally injected twice at 2 and 12 h after the onset of MCAO. Neuronal damage, brain edema and BBB permeability were measured 24 h following MCAO. Expression of MMP-9 protein and mRNA were determined by western blot and RT-PCR, respectively. Expression of tight junction protein (TJP) occludin was detected by western blot. Neuronal damage, brain edema and BBB permeability were significantly reduced by baicalin administration following focal cerebral ischemia. Elevated expression of MMP-9 protein and mRNA were significantly down-regulated by baicalin administration. In addition, MCAO caused the decreased expression of occludin, which was significantly up-regulated by baicalin administration. Our study suggested that baicalin reduces MCAO-induced neuronal damage, brain edema and BBB permeability, which might be associated with the inhibition of MMP-9 expression and MMP-9-mediated occludin degradation.

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Section: Discussionmentioning

confidence: 99%

Effect of Baicalin on Matrix Metalloproteinase-9 Expression and Blood–Brain Barrier Permeability Following Focal Cerebral Ischemia in Rats

Yang

Liang

et al. 2011

Neurochem Res

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“…Baicalin is a flavonoid that is a component of Scutellaria baicalensis Georgi roots, which have been widely used in China to treat stroke for thousands of years. This compound protected human SH-SY5Y neuroblastoma cells against A β -induced cytotoxicity and H 2 O 2 production [50]. Resveratrol is the most outstanding representative of wine polyphenols.…”

Section: Looking For New Neuroprotectantsmentioning

confidence: 99%

Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Therapeutic Perspectives

Melo

Monteiro

Lima

et al. 2011

Oxidative Medicine and Cellular Longevity

200

154

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The incidence and prevalence of neurodegenerative diseases (ND) increase with life expectancy. This paper reviews the role of oxidative stress (OS) in ND and pharmacological attempts to fight against reactive oxygen species (ROS)-induced neurodegeneration. Several mechanisms involved in ROS generation in neurodegeneration have been proposed. Recent articles about molecular pathways involved in ROS generation were reviewed. The progress in the development of neuroprotective therapies has been hampered because it is difficult to define targets for treatment and determine what should be considered as neuroprotective. Therefore, the attention was focused on researches about pharmacological targets that could protect neurons against OS. Since it is necessary to look for genes as the ultimate controllers of all biological processes, this paper also tried to identify gerontogenes involved in OS and neurodegeneration. Since neurons depend on glial cells to survive, recent articles about the functioning of these cells in aging and ND were also reviewed. Finally, clinical trials testing potential neuroprotective agents were critically reviewed. Although several potential drugs have been screened in in vitro and in vivo models of ND, these results were not translated in benefit of patients, and disappointing results were obtained in the majority of clinical trials.

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“…It is considered to be one of the effective and safe drugs widely used in Asia for the treatment of a variety of diseases, such as brain diseases, hepatic disorders, inflammatory diseases, and so on. Furthermore, it has been reported that baicalin has multiple biologic functions, including anti-inflammatory, antioxidant, antiapoptotic, and immune regulation properties (Xu et al, 2011;Yin et al, 2011;Hou et al, 2012). There is increasing evidence to support the notion that this compound may have potential roles in anti-inflammation and immune regulation (Liu et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Inhibitory Effect of Baicalin on Collagen-Induced Arthritis in Rats through the Nuclear Factor–κB Pathway

Wang

Huang

et al. 2014

J Pharmacol Exp Ther

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This study focused on the potential therapeutic effect of baicalin on collagen-induced arthritis (CIA) in rats and the underlying mechanisms. The CIA rats were injected with baicalin (50, 100, or 200 mg/kg) once daily for 30 days. The rats were monitored for clinical severity of arthritis, and joint tissues were used for radiographic assessment and histologic examination. We quantified tumor necrosis factor-a (TNF-a) and interleukin-1b (IL-1b) in experimental animals and used Western blots to assess levels of protein abundance, phosphorylation, and acetylation of nuclear factor (NF)-kB p65 and sirtuin 1 (sirt1) protein expression in joint tissues. Human fibroblast-like synoviocytes from rheumatoid arthritis (HFLS-RA) were adopted in further mechanistic investigations. Baicalin intraperitoneal injection for 30 days dose-dependently blocked clinical manifestations of CIA, such as functional impairment and swollen red paws. Meanwhile, it alleviated collageninduced joint inflammation injury and inhibited the secretion of TNF-a and IL-1b in both rat synovium and HFLS-RA. Further mechanistic investigations revealed that baicalin suppresses NF-kB p65 protein expression and phosphorylation in synovial tissue and human-derived synoviocytes. Moreover, the acetylation of NF-kB p65 was downregulated by baicalin, which negatively correlates with the baicalin-induced upregulation of sirt1 expression in the same conditions. The data indicate that CIA in rats can be alleviated by baicalin treatment via relieving joint inflammation, which is related to the suppression of synovial NF-kB p65 protein expression and the elevation of its deacetylation by sirt1.

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Baicalin prevents the production of hydrogen peroxide and oxidative stress induced by Aβ aggregation in SH-SY5Y cells

Cited by 64 publications

References 33 publications

Effect of Baicalin on Matrix Metalloproteinase-9 Expression and Blood–Brain Barrier Permeability Following Focal Cerebral Ischemia in Rats

Effect of Baicalin on Matrix Metalloproteinase-9 Expression and Blood–Brain Barrier Permeability Following Focal Cerebral Ischemia in Rats

Oxidative Stress in Neurodegenerative Diseases: Mechanisms and Therapeutic Perspectives

Inhibitory Effect of Baicalin on Collagen-Induced Arthritis in Rats through the Nuclear Factor–κB Pathway

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