rotenone/hemorrhage

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Vascular pathology in male Lewis rats following short-term, low-dose rotenone administration.

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The long-term administration of low doses of rotenone has been used to produce a model of Parkinson disease (PD) in rats. However, only about 50% of similarly treated rats develop the PD-like syndrome, with many dying during the first few days of treatment. The lesions in male Lewis rats that became

Vascular damage mediates neuronal and non-neuronal pathology following short and long-term rotenone administration in Sprague-Dawley rats.

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Even though rotenone has been used extensively in recent years to produce a model of Parkinson disease in rats, its systemic effects either on neurons apart from dopaminergic structures or non-neuronal tissues have not been elucidated well. In our present study, 30 adult Sprague-Dawley rats were

The first fatal case of yam bean and rotenone toxicity in Thailand.

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The first fatal case of Yam bean and Rotenone toxicity in Thailand was studied at Forensic Medicine, Chiang Mai, Thailand. A Chinese Taiwan man, 59 years old, was found dead after Yam bean ingestion. Yam bean toxicity and death have been found very rarely in the world and has not been reported in

Effect of nimodipine on mitochondrial respiration in different rat brain areas after subarachnoid haemorrhage.

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The mitochondrial respiration was evaluated in three different rat brain areas (cerebral cortex, hippocampus and brain stem) after experimental subarachnoid haemorrhage (SAH). The haemorrhage was induced by injecting 0.35 ml of autologous arterial blood into cisterna magna. Intravenous

NLRP3 inflammasome contributes to inflammation after intracerebral hemorrhage.

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OBJECTIVE The NLRP3 (NALP3, cryopyrin) inflammasome, a key component of the innate immune system, facilitates caspase-1 and interleukin (IL)-1β processing, which amplifies the inflammatory response. Here, we investigated whether NLRP3 knockdown decreases neutrophil infiltration, reduces brain edema,

Nesfatin-1 antagonized rotenone-induced neurotoxicity in MES23.5 dopaminergic cells.

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Nesfatin-1 is a recently identified brain-gut peptide involved in feeding and energy homeostasis. Recently, it has been proved that nesfatin-1 could exert its neuroprotective effect against subarachnoid hemorrhage-induced injury via its anti-apoptotic and anti-inflammatory properties. However,

Sodium Benzoate Attenuates Secondary Brain Injury by Inhibiting Neuronal Apoptosis and Reducing Mitochondria-Mediated Oxidative Stress in a Rat Model of Intracerebral Hemorrhage: Possible Involvement of DJ-1/Akt/IKK/NFκB Pathway.

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Intracerebral hemorrhage (ICH) is a devastating disease with high rates of mortality and morbidity. The aim of this study was to explore whether Sodium Benzoate (NaB) could reduce neural cell apoptosis and alleviate neurological deficits after ICH. To assess the therapeutic effects of NaB, first, we

Mdivi-1 ameliorates early brain injury after subarachnoid hemorrhage via the suppression of inflammation-related blood-brain barrier disruption and endoplasmic reticulum stress-based apoptosis.

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Aberrant modulation of mitochondrial dynamic network, which shifts the balance of fusion and fission towards fission, is involved in brain damage of various neurodegenerative diseases including Parkinson's disease, Huntington's disease and Alzheimer's disease. A recent research has shown that the

Mitochondrial inner membrane enzyme defects in porcine myocardial ischemia.

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Left anterior descending coronary artery occlusion in anesthetized pigs produced a stable transmural ischemia characterized by a rapid and then sustained loss of blood flow and mechanical function. After 2 h of occlusion, mitochondria from the ischemic area exhibited a 36 +/- 6% drop in state 3

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