Ginkgo biloba prevents transient global ischemia-induced delayed hippocampal neuronal death through antioxidant and anti-inflammatory mechanism

Tulsulkar, Jatin; Shah, Zahoor A.

doi:10.1016/j.neuint.2012.11.017

Cited by 67 publications

(48 citation statements)

References 37 publications

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“…Neuroinflammation can cause neuronal death, but also confers neuroprotection by triggering antioxidant defenses system in the damaged neurons (Stoll et al 2002). Nrf2 antioxidant signaling pathway is one of the most important activated antioxidant pathways during cerebral ischemia/reperfusion in the experimental and clinical trial studies (Tulsulkar and Shah 2012;Guo et al 2013). Besides, it was reported that antioxidant related enzymes such as superoxide dismutase; catalase and glutathione which are Nrf-2/β-actin (Arbitrary unit)…”

Section: Discussionmentioning

confidence: 99%

Pre-treatment with metformin activates Nrf2 antioxidant pathways and inhibits inflammatory responses through induction of AMPK after transient global cerebral ischemia

et al. 2014

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Global cerebral ischemia arises in patients who have a variety of clinical conditions including cardiac arrest, shock and asphyxia. In spite of advances in understanding of the brain ischemia and stroke etiology, therapeutic approaches to improve ischemic injury still remain limited. It has been established that metformin can attenuate cell death in cerebral ischemia. One of the main functions of metformin is proposed to be conducted via AMP-activated protein kinase (AMPK)-dependent pathway in the experimental cerebral ischemia model. It is also established that metformin can suppress inflammation and activate Nuclear factor erythroid 2-related factor (Nrf2) pathways in neurons. In the current study, the role of metformin in regulating inflammatory and antioxidant pathways in the global cerebral ischemia was investigated. Our results indicated that pretreatment of rats by metformin attenuated cellular levels of nuclear factor-κB, Tumor Necrosis Factor alpha and Cyclooxygenase-2 which are considered as three important proteins involved in the inflammation pathway. Pretreatment by metformin increased the level of Nrf2 and heme oxygenase-1 in the hippocampus of ischemic rats compared with untreated ischemic group. Moreover, pretreatment by metformin enhanced the level of glutathione and catalase activities compared with them in ischemic group. Such protective changes detected by metformin pretreatment were reversed by injecting compound c, an AMPK inhibitor. These findings suggested that metformin might protect cells through modulating inflammatory and antioxidant pathways via induction of AMPK. However, more experimental and clinical trial studies regarding neuroprotective potential of metformin and the involved mechanisms, especially in the context of cerebral ischemic injuries, are necessary.

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Section: Discussionmentioning

confidence: 99%

Pre-treatment with metformin activates Nrf2 antioxidant pathways and inhibits inflammatory responses through induction of AMPK after transient global cerebral ischemia

et al. 2014

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“…While the mechanisms responsible for cell loss during cerebral ischemia are not yet fully understood, much important work has been done on the subject in recent years (8,26). Histopathological studies performed with a cerebral ischemia model have determined pronounced contraction in neurons, irregularities in cell and nuclear margins, and perineural and pericapillary edema.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have investigated changes in the chemical structures of existing drugs used in treatment or the development of new drugs for that purpose, while there are also studies regarding various plant essences found in nature. One of the most important of these plants is Ginkgo biloba (GB) (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Effect of Ginkgo biloba on brain volume after carotid artery occlusion in rats: a stereological and histopathological study

Aktürk¹,

Odacı²,

İkinci³

et al. 2014

Turk J Med Sci

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“…The flavonoid glycosides confer antioxidant properties to ginkgo particularly at the mitochondrial level while the terpenoids act as antagonists of platelet-activating factor [45][46][47][48]. In comparison to other antioxidants such as vitamin C or vitamin E, the extracts of ginkgo can stabilize and protect mitochondrial function [49][50][51] thereby preventing oxidative damage to mitochondria [49].…”

Section: Ginkgo Bilobamentioning

confidence: 99%

Nutritional recommendations for individuals with Flammer syndrome

et al. 2017

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The Flammer syndrome (FS) describes the phenotype of people with a predisposition for an altered reaction of the blood vessels to stimuli like coldness or emotional stress.The question whether such people should be treated is often discussed. On the one hand, most of these subjects are healthy; on the other hand, FS seems to predispose to certain eye diseases such as normal tension glaucoma or retinitis pigmentosa or systemic diseases such as multiple sclerosis or tinnitus. A compromise between doing nothing and a drug treatment is the adaption of nutrition. But what do we mean by healthy food consumption for subjects with FS? The adaption of nutrition depends on the health condition. Whereas patients with e.g. a metabolic syndrome should reduce their calorie intake, this can be counterproductive for subjects with FS, as most subjects with FS have already a low body mass index (BMI) and the lower the BMI the stronger the FS symptoms. Accordingly, while fasting is healthy e.g. for subjects with metabolic syndrome, fasting can even dangerously aggravate the vascular dysregulation, as it has been nicely demonstrated by the loss of retinal vascular regulation during fasting. To give another example, while reducing salt intake is recommended for subjects with systemic hypertensions, such a salt restriction can aggravate systemic hypotension and thereby indirectly also the vascular regulation in subjects with FS. This clearly demonstrates that such a preventive adaption of nutrition needs to be personalized.

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Ginkgo biloba prevents transient global ischemia-induced delayed hippocampal neuronal death through antioxidant and anti-inflammatory mechanism

Cited by 67 publications

References 37 publications

Pre-treatment with metformin activates Nrf2 antioxidant pathways and inhibits inflammatory responses through induction of AMPK after transient global cerebral ischemia

Pre-treatment with metformin activates Nrf2 antioxidant pathways and inhibits inflammatory responses through induction of AMPK after transient global cerebral ischemia

Effect of Ginkgo biloba on brain volume after carotid artery occlusion in rats: a stereological and histopathological study

Nutritional recommendations for individuals with Flammer syndrome

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