Neuroprotective effects of berberine on stroke models in vitro and in vivo

Zhou, Xiqiao; Zeng, Xianlu; Kong, Hui; Sun, Xiu‐Lan

doi:10.1016/j.neulet.2008.09.064

Cited by 146 publications

(80 citation statements)

References 32 publications

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“…The increased concentration of ROS can cause cellular damage and subsequent cell death since ROS may oxidize crucial cellular components, including lipids, proteins and DNA (24). The levels of MDA and NO increased indicating that severe oxidative damage was caused by I/R (25).…”

Section: Discussionmentioning

confidence: 99%

α-lipoic acid protects against cerebral ischemia/reperfusion-induced injury in rats

Deng

Zuo

Zhang

et al. 2015

Molecular Medicine Reports

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Abstract. It is well established that the brain is sensitive to ischemia/reperfusion (I/R)-induced injury. α-lipoic acid (LA), a free radical scavenger and antioxidant, has a neuroprotective effect against cerebral I/R-induced injury, however, the underlying mechanisms remain to be elucidated. Therefore, the present study was undertaken to evaluate whether LA was able to protect against cerebral I/R-induced injury and to examine the potential mechanisms. The neuroprotective effects of LA were investigated in a rat model of transient focal ischemia induced by middle cerebral artery occlusion (MCAO) followed by reperfusion. Adult male Sprague-Dawley rats were randomly assigned into the sham, cerebral I/R injury model and model plus LA groups. Cerebral I/R injury was induced by 90 min MCAO followed by reperfusion for 24 h. Cerebral infarct size was detected by 2,3,5-triphenyltetrazolium chloride staining. Neurological deficit score (NDS), brain water content and oxidative parameters, including malondialdehyde (MDA), nitric oxide (NO), total antioxidant capacity (T-AOC) and superoxide dismutase (SOD) were measured. The expression of cleaved caspase-3, brain-derived neurotrophic factor (BDNF), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), p-Akt and phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) were also analyzed using western blotting. The present study demonstrated that pretreatment with LA significantly decreased the infarction size, brain water content and improved NDS. LA reversed the levels of oxidative parameters, including MDA, NO, T-AOC and SOD to their normal state in rat brains following cerebral I/R. Furthermore, the expression of cleaved caspase-3 markedly decreased and the expression of BDNF, PI3K, p-Akt and p-ERK1/2 significantly increased following administration of LA. On the basis of these findings, it was concluded that LA protected the brain from cerebral I/R damage by attenuation of oxidative stress and caspase-dependent apoptosis. Furthermore, LA exerts its neuroprotective effects potentially through activation of the BDNF-PI3K/Akt-ERK1/2 pathway. IntroductionCerebral ischemic injury is one of the leading causes of human mortality and disability worldwide (1). Restoration of blood flow to the ischemic brain is often used to treat patients in clinical experiments. However, reperfusion itself also has the potential to produce additional injuries in the ischemic brain due to overproduction of reactive oxygen species (ROS). The potential pathological mechanisms of ischemia/reperfusion (I/R) injury include glutamate excitotoxicity, calcium overload, nitric oxide (NO) production, oxidative stress, inflammation and apoptosis, which eventually lead to cell death (2). Oxidative stress and apoptosis following cerebral I/R are the two major processes that induce neuronal injury (3,4). For this reason, multifunctional molecules with anti-oxidative and anti-apoptotic properties are ideal neuroprotective agents.α-lipoic acid (LA), an endogenous short-chain fatty acid, is a cofact...

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Section: Discussionmentioning

confidence: 99%

α-lipoic acid protects against cerebral ischemia/reperfusion-induced injury in rats

Deng

Zuo

Zhang

et al. 2015

Molecular Medicine Reports

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“…It shows a trend of increasing incidence rate each year and has become one of the major diseases with high morbidity and mortality (Zhou et al 2008;Lakhan et al 2009;Wu et al 2010). Recent studies on the mechanism of ischemic brain injury have made rapid progress, demonstrating that factors such as neuronal damage caused by free radicals, excitatory amino acid toxicity, inflammation and cell apoptosis play important roles during the process of ischemic brain injury (Ritz et al 2008;Mukerji et al 2009).…”

Section: Introductionmentioning

confidence: 99%

The protective effect of qiancao naomaitong mixture on neuronal damage and cerebral ischemia/reperfusion injury

Lü

Zhan

et al. 2016

Pharmaceutical Biology

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Context Qiancao Naomaitong Mixture (QNM) is mainly used to treat ischemic stroke patients in the clinic. Objective This study evaluates the protective effect of QNM on neuronal damage in vitro, and clarifies the underlying mechanism against cerebral ischemia-reperfusion (I/R) injury in vivo. Materials and methods Activity assay of caspase 3 (C-3) and caspase 8 (C-8) were measured with microplate reader and cell apoptosis was investigated. Cerebral I/R injury was induced by MCAO model. QNM groups were given at 0.27, 0.54 and 1.08 mL/100 g body weight. The weight ratio of cerebral infarction tissue was obtained. The cytokine levels in serum and brain tissue were measured using ELISA.

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“…Some studies have shown that natural products of plant origin can prevent neuronal cell death (4,20,21). Withania coagulans has many properties, such as anti-inflammatory, antiapoptotic and neuroregeneration effects (8).…”

Section: Discussionmentioning

confidence: 99%

Withania coagulans Extract Attenuates Histopathological Alteration and Apoptosis in Rat Brain Cortex Following Ischemia/Reperfusion Injury

2016

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Background: Cerebral ischemia and reperfusion (I/R) is a pathological condition that arises by reduction or cessation in cerebral blood flow and return of oxygen and metabolites to brain cells, which cause oxidative damage. Objectives: The aim of this study was to investigate the neuroprotective effects of Withania coagulans (WC) extract on brain cortex in a rat model of I/R. Materials and Methods: Thirty-two adult male Wistar rats weighing 280 -300 g were used in this study. Animals were randomly divided to four groups (n = 8) as follow: sham operated group (I), I/R group (II), WCE500 + I/R (III) and WCE1000 + I/R groups (IV). Pretreatment with WC extract (500, 1000 mg/kg) was done by oral gavage for 30 days and global brain ischemia was induced by the common carotid occlusion for 30 minutes. After 72 hours, the animals were perfused transcardially and then the brains were prepared for histological study (H & E and TUNEL staining). Results: The I/R group showed a significant increase in pycnotic (dying) neurons and pretreatment with WC at doses of 500 mg/kg and 1000 mg/kg significantly reduced pycnotic and TUNEL positive neurons, in a dose dependent manner in ischemic brain cortex. Conclusions: Our findings indicated that WC has neuroprotective effects and is able to reduce histopathological alterations and apoptosis in brain cortex I/R in rats.

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Neuroprotective effects of berberine on stroke models in vitro and in vivo

Cited by 146 publications

References 32 publications

α-lipoic acid protects against cerebral ischemia/reperfusion-induced injury in rats

α-lipoic acid protects against cerebral ischemia/reperfusion-induced injury in rats

The protective effect of qiancao naomaitong mixture on neuronal damage and cerebral ischemia/reperfusion injury

Withania coagulans Extract Attenuates Histopathological Alteration and Apoptosis in Rat Brain Cortex Following Ischemia/Reperfusion Injury

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