Correction to: Nitric Oxide Participates in the Brain Ischemic Tolerance Induced by Intermittent Hypobaric Hypoxia in the Hippocampal CA1 Subfield in Rats

Abstract The study explored the effect of chronic intermittent hypobaric hypoxia (CIHH) on osteoarthritis (OA). CIHH conditioning was realized by exposing rats to hypobaric hypoxia environment mimicking 5,000 m high-altitude (PB=404 mmHg, PO2=84 mmHg) 6 h per day, once daily for 28 days. OA model was induced by surgically-induced medial meniscal tear. Male Wistar rats were randomly assigned into 5 groups: preconditioning group （CIHH + OA）, postconditioning group （OA + CIHH）, control group, inhibitor group [OA + inducible nitric oxide synthase (iNOS) inhibitor], blank control group. The expression iNOS, nitric oxide (NO) content levels in the joint fluid were measured at 1, 2, 3 weeks after the OA modelling. Results revealed that OA modelling induced cartilage degeneration, up-regulated iNOS expression, increased joint fluid NO content. CIHH preconditioning and postconditioning reduced cartilage degeneration, prevented the NO production. Inhibitor groups showed alleviated joint degeneration than control group, but not as effective as CIHH condition. These results suggest that both CIHH preconditioning and postconditioning plays a protective role on OA, one of the mechanism was inhibiting the overexpression of iNOS and NO production.

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Hippocampal Damage following Repeated Brief Hypotensive Episodes in the Rat

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1991.163 ◽

1991 ◽

Vol 11 (6) ◽

pp. 974-978 ◽

Cited By ~ 7

Author(s):

Yoichi Yamauchi ◽

Hiroyuki Kato ◽

Kyuya Kogure

Keyword(s):

Brain Damage ◽

Neuronal Damage ◽

Neuronal Loss ◽

Hippocampal Damage ◽

Shed Blood ◽

Arterial Blood ◽

Hippocampal Ca1 ◽

Severe Hypotension ◽

The Brain ◽

Hippocampal Ca1 Subfield

We examined the brain damage following repeated hypotensive episodes in the rat. Severe hypotension was induced by withdrawal of arterial blood. The MABP was maintained at about 25 mm Hg with isoelectric EEG and the shed blood was retransfused. After 1 week of recovery, histopathological changes were examined. No brain damage was observed after 1 min of isoelectric EEG. Mild neuronal damage to the hippocampal CA1 subfield was seen in some animals after two episodes of 1-min isoelectric EEG at a 1-h interval. Significant and consistent neuronal loss in the hippocampal CA1 subfield was observed after three episodes of 1-min isoelectric EEG. Scattered neuronal damage in the thalamus was additionally seen in some animals. The present study indicates that repeated brief hypotensive episodes produce brain damage depending on the number of episodes, even though no brain damage results when induced as a single insult. This animal model may reproduce hemodynamic transient ischemic attacks in humans.

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Quercetin Ameliorate Oxidative/Nitrosative Stress in The Brain of Rats Exposed to Intermittent Hypobaric Hypoxia

Revista Virtual de Química ◽

10.5935/1984-6835.20160027 ◽

2016 ◽

Vol 8 (2) ◽

pp. 369-383 ◽

Cited By ~ 1

Author(s):

Irina Camelia Chiş ◽

Doina Baltaru ◽

Anca Dumitrovici ◽

Andrei Coseriu ◽

Bogdan Cristian Radu ◽

...

Keyword(s):

Hypobaric Hypoxia ◽

Nitrosative Stress ◽

Intermittent Hypobaric Hypoxia ◽

The Brain

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Effect of Polygala tenuifolia Root Extract on Cerebral Ischemia and Reperfusion

The American Journal of Chinese Medicine ◽

10.1142/s0192415x06003680 ◽

2006 ◽

Vol 34 (01) ◽

pp. 115-123 ◽

Cited By ~ 8

Author(s):

Jin-Hyuk Park ◽

Jin Sook Kim ◽

Dae Sik Jang ◽

Sun-Mee Lee

Keyword(s):

Lipid Peroxidation ◽

Cerebral Ischemia ◽

Ethanol Extract ◽

Root Extract ◽

Ischemia And Reperfusion ◽

Butanol Fraction ◽

Hippocampal Ca1 ◽

Polygala Tenuifolia ◽

The Brain ◽

Hippocampal Ca1 Subfield

In this study, the effects of Polygala tenuifolia root extract on brain ischemia/reperfusion injury in Mongolian gerbils were investigated. The gerbils were administered ethanol extract of P. tenuifolia and its four sub-fractions orally 2 hours prior to ischemia, and were subjected to a 20-minute no-flow cerebral ischemia in vivo. Thirty minutes and 72 hours after reperfusion, the brain was removed and the ATP, lactate and lipid peroxide levels were determined, and the neurons in the hippocampal CA1 subfield were examined. In the vehicle-treated ischemic gerbils, the brain ATP levels decreased significantly, but this decrease was prevented by pre-treatment with an n-butanol fraction of P. tenuifolia. In contrast, both the lactate content and lipid peroxidation levels were elevated in the vehicle-treated ischemic animals, but this elevation was inhibited by ethanol extract and n-butanol fraction of P. tenuifolia, respectively. Both the ethanol extract and n-butanol fraction of P. tenuifolia attenuated post-ischemic neuronal necrosis in the hippocampal CA1 subfield. Our findings suggest that both ethanol extract and n-butanol fraction of P. tenuifolia root can reduce brain damage during ischemia and reperfusion, and prevent lipid peroxidation and preserve the energy metabolism.

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