Neuroprotective Effects of Scutellarin against Hypoxic-Ischemic-Induced Cerebral Injury via Augmentation of Antioxidant Defense Capacity

Berberine exerts neuroprotective and modulates hypoxia inducible factor-1-alpha (HIF-1[Formula: see text]. Based on the role of HIF-1[Formula: see text] in hypoxia preconditioning and association between HIF-1[Formula: see text] and sphingosine-1-phosphate (S1P), we hypothesized that berberine preconditioning (BP) would ameliorate the cerebral injury induced by ischemia through activating the system of HIF-1[Formula: see text] and S1P. Adult male rats with middle cerebral artery occlusion (MCAO) and rat primary cortical neurons treated with oxygen and glucose deprivation (OGD) with BP at 24[Formula: see text]h (40[Formula: see text]mg/kg) and 2[Formula: see text]h (10[Formula: see text][Formula: see text]mol/L), respectively, were used to determine the neuroprotective effects. The HIF-1[Formula: see text] accumulation, and S1P metabolism were assayed in the berberine-preconditioned neurons, and the HIF-1[Formula: see text]-mediated transcriptional modulation of sphingosine kinases (Sphk) 1 and 2 was analyzed using chromatin immunoprecipitation and real-time polymerase chain reaction. BP significantly prevented cerebral ischemic injury in the MCAO rats at 24[Formula: see text]h and 72[Formula: see text]h following ischemia/reperfusion. In OGD-treated neurons, BP enhanced HIF-1[Formula: see text] accumulation with activation of PI3K/Akt, and induced S1P production by activating Sphk2 via the promotion of HIF-1[Formula: see text]-mediated Sphk2 transcription. In conclusion, BP activated endogenous neuroprotective mechanisms associated with the S1P/HIF-1 pathway and helped protect neuronal cells against hypoxia/ischemia.

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Sevoflurane Preconditioning against Focal Cerebral Ischemia

Anesthesiology ◽

10.1097/aln.0b013e3181a1fe68 ◽

2009 ◽

Vol 110 (6) ◽

pp. 1271-1278 ◽

Cited By ~ 59

Author(s):

Jean-Laurent Codaccioni ◽

Lionel J. Velly ◽

Chahrazad Moubarik ◽

Nicolas J. Bruder ◽

Pascale S. Pisano ◽

...

Keyword(s):

Cerebral Ischemia ◽

Focal Cerebral Ischemia ◽

Infarct Volume ◽

Cerebral Injury ◽

Terminal Deoxynucleotidyl Transferase ◽

Control Group ◽

Sprague Dawley ◽

Nissl Staining ◽

Neuroprotective Effects ◽

Sevoflurane Preconditioning

Background Preconditioning the brain with volatile anesthetics seems to be a viable option for reducing ischemic cerebral injury. However, it is uncertain whether this preconditioning effect extends over a longer period of time. The purpose of this study was to determine if sevoflurane preconditioning offers durable neuroprotection against cerebral ischemia. Methods Rats (Sprague-Dawley) were randomly allocated to two groups: nonpreconditioned control group (n = 44) and preconditioned group (n = 45) exposed to 2.7 vol% sevoflurane (45 min) 60 min before surgery. Animals in both groups were anesthetized with 3.0 vol% sevoflurane and subjected to transient middle cerebral artery occlusion. After 60 min of awake focal ischemia, the filament was removed. Functional neurologic outcome (range 0-18; 0 = no deficit), cerebral infarct size (Nissl staining), and apoptosis (Terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick-end labeling; cleaved caspase-3 staining) were evaluated at 3, 7, and 14 days after ischemia. Results Sevoflurane preconditioning significantly improved functional outcome and reduced infarct volume (109 +/- 43 vs. 148 +/- 56 mm(3)) 3 days after ischemia compared to the control group. However, after 7- and 14-day recovery periods, no significant differences were observed between groups. The number of apoptotic cells was significantly lower in the preconditioned group than in the control group after 3- and 7-day recovery periods. Fourteen days after ischemia, no differences were observed between groups. Conclusion In this model of transient focal cerebral ischemia, sevoflurane preconditioning induced effective but transient neuroprotective effects. Sevoflurane preconditioning also decreased ischemia-induced apoptosis in a more sustained way because it was observed up to 7 days after injury.

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Blood Schizonticidal Activity of Phyllanthus amarus Enhances Testovarian Antioxidant Defense Capacity in Plasmodium berghei Infected Mice

Tropical Journal of Natural Product Research ◽

10.26538/tjnpr/v2i3.10 ◽

2018 ◽

Vol 2 (3) ◽

pp. 150-157

Author(s):

Theresa Ezedom ◽

◽

Olukemi Opajobi ◽

Innocent Onyesom ◽

Lilian Chris-Ozoko ◽

...

Keyword(s):

Plasmodium Berghei ◽

Antioxidant Defense ◽

Phyllanthus Amarus ◽

Antioxidant Defense Capacity

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A Critical Review of the Abilities, Determinants, and Possible Molecular Mechanisms of Seaweed Polysaccharides Antioxidants

International Journal of Molecular Sciences ◽

10.3390/ijms21207774 ◽

2020 ◽

Vol 21 (20) ◽

pp. 7774

Author(s):

Zhiwei Liu ◽

Xian Sun

Keyword(s):

Antioxidant Defense ◽

Molecular Mechanisms ◽

Mechanisms Of Action ◽

Oxygen Species ◽

Good Potential ◽

Antioxidant Defense Capacity ◽

Main Components ◽

Excessive Proliferation ◽

Excess Reactive Oxygen Species ◽

Cancer Diseases

Oxidative stress induces various cardiovascular, neurodegenerative, and cancer diseases, caused by excess reactive oxygen species (ROS). It is attributed to the lack of sufficient antioxidant defense capacity to eliminate unnecessary ROS. Seaweeds are largely cultivated for their edible and commercial purposes. Excessive proliferation of some seaweeds has occurred in coastal areas, causing environmental and economic disasters, and even threating human health. Removing and disposing of the excess seaweeds are costly and labor-intensive with few rewards. Therefore, improving the value of seaweeds utilizes this resource, but also deals with the accumulated biomass in the environment. Seaweed has been demonstrated to be a great source of polysaccharides antioxidants, which are effective in enhancing the antioxidant system in humans and animals. They have been reported to be a healthful method to prevent and/or reduce oxidative damage. Current studies indicate that they have a good potential for treating various diseases. Polysaccharides, the main components in seaweeds, are commonly used as industrial feedstock. They are readily extracted by aqueous and acetone solutions. This study attempts to review the current researches related to seaweed polysaccharides as an antioxidant. We discuss the main categories, their antioxidant abilities, their determinants, and their possible molecular mechanisms of action. This review proposes possible high-value ways to utilize seaweed resources.

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Pharmacological connection of Histamine-1 (H1) Receptor Mediated Neuroprotective mechanism of Ischemic preconditioning in rat

Research Journal of Pharmacy and Technology ◽

10.52711/0974-360x.2021.00479 ◽

2021 ◽

pp. 2717-2722

Author(s):

Prabhat Singh ◽

Bhupesh Sharma

Keyword(s):

Cerebral Ischemia ◽

Cerebral Infarction ◽

Ischemic Preconditioning ◽

Ischemia Reperfusion ◽

Cerebral Injury ◽

Cerebral Stroke ◽

H1 Receptor ◽

Neuroprotective Effects ◽

Motor Incoordination ◽

Nitrite Nitrate

Cerebral ischemia and ischemia-reperfusion is an essential contributor to acute cerebral stroke. Ischemic preconditioning (IPC) has been proven to provide neuroprotection in ischemia-reperfusion injury in rats, but their mechanism behind neuroprotection in cerebral stroke are still unclear. Central histaminergic pathway has crucial role in the pathogenesis of cerebral stroke, but their neuroprotective role in IPC is still unidentified. This research explores the role of histamine-1 receptor in IPC induced neuroprotection against ischemia-reperfusion induced cerebral injury. Rat were subjected to 17 min of global cerebral ischemia (GCI) by occluding both carotid arteries followed by reperfusion for 24 h, to produce ischemia-reperfusion induced cerebral injury. TTC staining was used to measure cerebral infarct size. Morris water maze test was used to assess memory. Inclined beam-walk, hanging wire, lateral push and rota-rod tests were used to assess degree of motor incoordination. Brain acetylcholinesterase activity, nitrite/nitrate, glutathione, TBARS and MPO levels were also examined. GCI has produced a significant increase in cerebral infarction, brain nitrite/nitrate, MPO, TBARS and AChE activity along with a reduction in glutathione content. Impairment of memory and motor coordination were also noted in GCI induced rat. IPC was employed that consist of 3 preceding episodes of ischemia (1 min) and reperfusion (1 min) both immediately before GCI significantly decreased cerebral infarction, motor incoordination, memory impairment and biochemical impairment. Pretreatment with L-histidine mimicked the neuroprotective effects of IPC. L-histidine induced neuroprotection were significantly abolished by chlorpheniramine, a H1 receptor antagonist. We conclude that neuroprotective effects of IPC, probably occurs through the central histaminergic pathway, and histamine-1 receptor could be a new target behind the neuroprotective mechanism of IPC.

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