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An antioxidant phytotherapy to rescue neuronal oxidative stress.

Lin Z, Zhu D, Yan Y, Yu B, Wang Q, Shen P, Ruan K - Evid Based Complement Alternat Med (2011)

Bottom Line: The neurological deficit and brain infarction were also significantly elevated by MCAO as compared with sham-operated group.All the brain oxidative stress and damage were significantly attenuated by 7 days pretreatment with the aqueous extract of FBD (250 mg kg(-1), p.o.).In conclusion, FBD was a distinct antioxidant phytotherapy to rescue neuronal oxidative stress, through blocking LPO, restoring endogenous antioxidant system, but not scavenging free radicals.

View Article: PubMed Central - PubMed

Affiliation: Department of Chinese Medicinal Prescription, China Pharmaceutical University, 639 Longmian Avenue, Jiangning University City, Nanjing, Jiangsu 211198, China.

ABSTRACT
Oxidative stress is involved in the pathogenesis of ischemic neuronal injury. A Chinese herbal formula composed of Poria cocos (Chinese name: Fu Ling), Atractylodes macrocephala (Chinese name: Bai Zhu) and Angelica sinensis (Chinese names: Danggui, Dong quai, Donggui; Korean name: Danggwi) (FBD), has been proved to be beneficial in the treatment of cerebral ischemia/reperfusion (I/R).This study was carried out to evaluate the protective effect of FBD against neuronal oxidative stress in vivo and in vitro. Rat I/R were established by middle cerebral artery occlusion (MCAO) for 1 h, followed by 24 h reperfusion. MCAO led to significant depletion in superoxide dismutase and glutathione and rise in lipid peroxidation (LPO) and nitric oxide in brain. The neurological deficit and brain infarction were also significantly elevated by MCAO as compared with sham-operated group. All the brain oxidative stress and damage were significantly attenuated by 7 days pretreatment with the aqueous extract of FBD (250 mg kg(-1), p.o.). Moreover, cerebrospinal fluid sampled from FBD-pretreated rats protected PC12 cells against oxidative insult induced by 0.2 mM hydrogen peroxide, in a concentration and time-dependent manner (IC(50) 10.6%, ET(50) 1.2 h). However, aqueous extract of FBD just slightly scavenged superoxide anion radical generated in xanthine-xanthine oxidase system (IC(50) 2.4 mg ml(-1)) and hydroxyl radical generated in Fenton reaction system (IC(50) 3.6 mg ml(-1)). In conclusion, FBD was a distinct antioxidant phytotherapy to rescue neuronal oxidative stress, through blocking LPO, restoring endogenous antioxidant system, but not scavenging free radicals.

No MeSH data available.


Related in: MedlinePlus

Effect of rat CSF-FBD on PC12 cells induced by hydrogen peroxide. All the data were shown as the mean ± SD, n = 6. Significance was evaluated with one-way ANOVA following by two-sided Dunnett's t-test.*P < .05, **P < .1, ***P < .001versus blank CSF.
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fig2: Effect of rat CSF-FBD on PC12 cells induced by hydrogen peroxide. All the data were shown as the mean ± SD, n = 6. Significance was evaluated with one-way ANOVA following by two-sided Dunnett's t-test.*P < .05, **P < .1, ***P < .001versus blank CSF.

Mentions: Incubation with H2O2 for 3 h significantly reduced cell viability. However, when the cells were treated with rat CSF-FBD, the observed cell toxicity was significantly attenuated. As illustrated in Figure 2, CSF-FBD markedly reduced H2O2 injury within 1.5 h in a time-dependent manner (ET50 1.2 h) and concentration-dependant manner within 20% (IC50 10.6%). Meanwhile, blank CSF had no obvious influence on the control PC12 cells and Vit E (10 mM) protected PC12 cells by only 25.2%.


An antioxidant phytotherapy to rescue neuronal oxidative stress.

Lin Z, Zhu D, Yan Y, Yu B, Wang Q, Shen P, Ruan K - Evid Based Complement Alternat Med (2011)

Effect of rat CSF-FBD on PC12 cells induced by hydrogen peroxide. All the data were shown as the mean ± SD, n = 6. Significance was evaluated with one-way ANOVA following by two-sided Dunnett's t-test.*P < .05, **P < .1, ***P < .001versus blank CSF.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3139923&req=5

fig2: Effect of rat CSF-FBD on PC12 cells induced by hydrogen peroxide. All the data were shown as the mean ± SD, n = 6. Significance was evaluated with one-way ANOVA following by two-sided Dunnett's t-test.*P < .05, **P < .1, ***P < .001versus blank CSF.
Mentions: Incubation with H2O2 for 3 h significantly reduced cell viability. However, when the cells were treated with rat CSF-FBD, the observed cell toxicity was significantly attenuated. As illustrated in Figure 2, CSF-FBD markedly reduced H2O2 injury within 1.5 h in a time-dependent manner (ET50 1.2 h) and concentration-dependant manner within 20% (IC50 10.6%). Meanwhile, blank CSF had no obvious influence on the control PC12 cells and Vit E (10 mM) protected PC12 cells by only 25.2%.

Bottom Line: The neurological deficit and brain infarction were also significantly elevated by MCAO as compared with sham-operated group.All the brain oxidative stress and damage were significantly attenuated by 7 days pretreatment with the aqueous extract of FBD (250 mg kg(-1), p.o.).In conclusion, FBD was a distinct antioxidant phytotherapy to rescue neuronal oxidative stress, through blocking LPO, restoring endogenous antioxidant system, but not scavenging free radicals.

View Article: PubMed Central - PubMed

Affiliation: Department of Chinese Medicinal Prescription, China Pharmaceutical University, 639 Longmian Avenue, Jiangning University City, Nanjing, Jiangsu 211198, China.

ABSTRACT
Oxidative stress is involved in the pathogenesis of ischemic neuronal injury. A Chinese herbal formula composed of Poria cocos (Chinese name: Fu Ling), Atractylodes macrocephala (Chinese name: Bai Zhu) and Angelica sinensis (Chinese names: Danggui, Dong quai, Donggui; Korean name: Danggwi) (FBD), has been proved to be beneficial in the treatment of cerebral ischemia/reperfusion (I/R).This study was carried out to evaluate the protective effect of FBD against neuronal oxidative stress in vivo and in vitro. Rat I/R were established by middle cerebral artery occlusion (MCAO) for 1 h, followed by 24 h reperfusion. MCAO led to significant depletion in superoxide dismutase and glutathione and rise in lipid peroxidation (LPO) and nitric oxide in brain. The neurological deficit and brain infarction were also significantly elevated by MCAO as compared with sham-operated group. All the brain oxidative stress and damage were significantly attenuated by 7 days pretreatment with the aqueous extract of FBD (250 mg kg(-1), p.o.). Moreover, cerebrospinal fluid sampled from FBD-pretreated rats protected PC12 cells against oxidative insult induced by 0.2 mM hydrogen peroxide, in a concentration and time-dependent manner (IC(50) 10.6%, ET(50) 1.2 h). However, aqueous extract of FBD just slightly scavenged superoxide anion radical generated in xanthine-xanthine oxidase system (IC(50) 2.4 mg ml(-1)) and hydroxyl radical generated in Fenton reaction system (IC(50) 3.6 mg ml(-1)). In conclusion, FBD was a distinct antioxidant phytotherapy to rescue neuronal oxidative stress, through blocking LPO, restoring endogenous antioxidant system, but not scavenging free radicals.

No MeSH data available.


Related in: MedlinePlus