Effect of Gastrodin on Early Brain Injury and Neurological Outcome After Subarachnoid Hemorrhage in Rats

Wang, Xinzhi; Li, Shuyue; Ma, Jinbang; Chuan-gang, Wang; Chen, Anzhong; Xin, Zhen-xue; Zhang, Jianjun

doi:10.1007/s12264-018-00333-w

Cited by 40 publications

(23 citation statements)

References 26 publications

(35 reference statements)

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“…Nevertheless, GAS could alleviate motor performance in cerebral palsy patients and rescue cell death in macrophages by inhibiting oxidative stress [ 31 ]. GAS treatment increased blood-brain barrier permeability and attenuated subarachnoid hemorrhage induced brain damage by decreasing the oxidative stress and inflammation in rats [ 6 ]. At present, our results also found that Pb exposure increased MDA level and decreased the activities of SOD and TAC ( Table 2 ), which could contribute to its pathogenesis by disrupting the pro-/antioxidant balance in cells and decreases the activities of several antioxidant enzymes [ 8 , 30 ].…”

Section: Discussionmentioning

confidence: 99%

“…The choice of Pb dose was based on previous reports [ 8 , 12 ]. The dose of GAS selected in this study was based on previously published data on the neuroprotective effect of GAS [ 1 , 6 ].…”

Section: Methodsmentioning

confidence: 99%

“…Previous studies have indicated that GAS treatment alleviated memory deficits by increasing the expression of NR2A and GluR2 in the cerebellum of diabetic rats [ 5 ]. GAS treatment ameliorates subarachnoid hemorrhage induced neurological deficit, oxidative stress, inflammation and apoptosis by increasing Nrf2 activation and suppressing the expressions of interleukin (IL)-1β and tumor necrosis factor (TNF)-α [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

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Effects of Gastrodin against Lead-Induced Brain Injury in Mice Associated with the Wnt/Nrf2 Pathway

et al. 2020

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Gastrodin (GAS), the main phenolic glycoside extracted from Gastrodia elata Blume, exhibited potential neuroprotective properties. Here we examined the protective effects of GAS against lead(Pb)-induced nerve injury in mice, and explores its underlying mechanisms. Our research findings revealed that GAS improved behavioral deficits in Pb-exposed mice. GAS reduced the accumulation of p-tau and amyloid-beta (Aβ). GAS inhibited Pb-induced inflammation in the brain, as indicated by the decreased levels of pro-inflammatory cytokines, including tumor necrosis factor-a (TNF-α), cyclooxygenase-2 (COX-2). GAS increased the expression levels of NR2A and neurotrophin brain-derived neurotrophic factor (BDNF). GAS inhibited Pb-induced apoptosis of neurons in hippocampus tissue, as indicated by the decreased levels of pro-apoptotic proteins Bax and cleaved caspase-3. Furthermore, the neuroprotective effects of GAS were associated with inhibiting oxidative stress by modulating nuclear factor-erythroid 2-related factor 2 (Nrf2)-mediated antioxidant signaling. GAS supplement activated the Wnt/β-catenin signaling pathway and reduced the expression of Wnt inhibitor Dickkopf-1 (Dkk-1). Collectively, this study clarified that GAS exhibited neuroprotective property by anti-oxidant, anti-inflammatory and anti-apoptosis effects and its ability to regulate the Wnt/Nrf2 pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of Gastrodin against Lead-Induced Brain Injury in Mice Associated with the Wnt/Nrf2 Pathway

et al. 2020

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“…Currently, new insight suggests that EBI within 72 hours after SAH onset may lay the foundation for subsequent pathophysiological changes and poor outcomes of patients. The pathological mechanisms of EBI include oxidative stress, platelet activation, in ammation, and neuronal apoptosis [34][35][36][37]. One animal experiment found that hyperglycemia could increase reactive oxygen species (ROS) production through activating protein kinase C after stroke, thereby exacerbating oxidative stress [38].…”

Section: Discussionmentioning

confidence: 99%

Effect of stress-induced hyperglycemia after non-traumatic non-aneurysmal subarachnoid hemorrhage on clinical complications and functional outcomes

Zhang

Zhao

Liu

et al. 2021

Preprint

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Background Despite having an overall benign course, non-traumatic non-aneurysmal subarachnoid hemorrhage (naSAH) is still accompanied by a risk of clinical complications and poor outcomes. Risk factors and mechanisms of complications and poor outcomes after naSAH remain unknown. Our aim was to explore the effect of stress-induced hyperglycemia (SIH) on complication rates and functional outcomes in naSAH patients. Methods We retrospectively reviewed patients with naSAH admitted to our institution between 2013 and 2018. SIH was identified according to previous criterion. Symptomatic vasospasm, delayed cerebral infarction, and hydrocephalus were identified as main complications. Outcomes were reviewed using a modified Rankin Scale (mRS) at discharge, 3 months, and 12 months. A statistical analysis of clinical, radiological, and laboratory risk factors of complications and outcomes was conducted. Results 244 naSAH patients were incorporated in the cohort with 74 (30.3%) SIH. After adjusting for age, gender, hypertension, Hunt and Hess (HH) grade, modified Fisher Scale (mFS), intraventricular hemorrhage (IVH), and subarachnoid blood distribution, SIH was significantly associated with symptomatic vasospasm (P < 0.001, 12.176 [4.904–30.231]), delayed cerebral infarction (P < 0.001, 12.434 [3.850-40.161]), hydrocephalus (P = 0.008, 5.771 [1.570-21.222]), and poor outcome at 12 months (P = 0.006, 5.506 [1.632–18.581]), whereas the correlation between SIH and poor outcome at discharge (P = 0.064, 2.409 [0.951-6.100]) or 3 months (P = 0.110, 2.029 [0.852–4.833]) was not significant. Incorporation of SIH increased the area under curve (AUC) of ROC in the combined model for predicting symptomatic vasospasm (P = 0.002), delayed cerebral infarction (P = 0.024), hydrocephalus (P = 0.037), and 12-month poor outcome (P = 0.087). Conclusions SIH is a significant and independent risk factor for symptomatic vasospasm, delayed cerebral infarction, hydrocephalus, and long-term poor outcome in naSAH patients. Identifying SIH early after naSAH is important for decision-making and treatment planning.

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“…Telmisartan [ 225 ], nebivolol [ 226 ] and curcumin [ 227 ] can ameliorate cerebral vasospasm, and Pterostilbene can attenuate EBI by inhibiting the NLRP3 inflammasome [ 228 ]. Some antioxidants (e.g., apigenin [ 229 ], peroxiredoxin1/2 [ 230 ], docosahexaenoic acid [ 231 ], sodium hydrosulfide [ 232 ], cysteamine [ 233 ], gastrodin [ 234 ], naringin [ 60 ], and progesterone [ 235 ]) play a neuroprotective role in EBI through the effects of anti-apoptosis after SAH, but other antioxidants (e.g. AVE 0991 and mangiferin [ 56 , 236 ] memantine [ 59 , 237 ], salvianolic acid B [ 238 , 239 ], salvianolic acid A [ 240 ], and allicin [ 241 ]) protect against SAH-induced oxidative injury via inhibition of oxidative, inflammatory, and apoptotic pathways.…”

Section: Antioxidants and Antidepressants In Stroke/depressionmentioning

confidence: 99%

Oxidative Stress at the Crossroads of Aging, Stroke and Depression

et al. 2020

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Epidemiologic studies have shown that in the aging society, a person dies from stroke every 3 minutes and 42 seconds, and vast numbers of people experience depression around the globe. The high prevalence and disability rates of stroke and depression introduce enormous challenges to public health. Accumulating evidence reveals that stroke is tightly associated with depression, and both diseases are linked to oxidative stress (OS). This review summarizes the mechanisms of OS and OS-mediated pathological processes, such as inflammation, apoptosis, and the microbial-gut-brain axis in stroke and depression. Pathological changes can lead to neuronal cell death, neurological deficits, and brain injury through DNA damage and the oxidation of lipids and proteins, which exacerbate the development of these two disorders. Additionally, aging accelerates the progression of stroke and depression by overactive OS and reduced antioxidant defenses. This review also discusses the efficacy and safety of several antioxidants and antidepressants in stroke and depression. Herein, we propose a crosstalk between OS, aging, stroke, and depression, and provide potential therapeutic strategies for the treatment of stroke and depression.

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Effect of Gastrodin on Early Brain Injury and Neurological Outcome After Subarachnoid Hemorrhage in Rats

Cited by 40 publications

References 26 publications

Effects of Gastrodin against Lead-Induced Brain Injury in Mice Associated with the Wnt/Nrf2 Pathway

Effects of Gastrodin against Lead-Induced Brain Injury in Mice Associated with the Wnt/Nrf2 Pathway

Effect of stress-induced hyperglycemia after non-traumatic non-aneurysmal subarachnoid hemorrhage on clinical complications and functional outcomes

Oxidative Stress at the Crossroads of Aging, Stroke and Depression

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