Italian
Albanian
Arabic
Armenian
Azerbaijani
Belarusian
Bengali
Bosnian
Catalan
Czech
Danish
Deutsch
Dutch
English
Estonian
Finnish
Français
Greek
Haitian Creole
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Irish
Italian
Japanese
Korean
Latvian
Lithuanian
Macedonian
Mongolian
Norwegian
Persian
Polish
Portuguese
Romanian
Russian
Serbian
Slovak
Slovenian
Spanish
Swahili
Swedish
Turkish
Ukrainian
Vietnamese
Български
中文(简体)
中文(繁體)
Molecular Neurobiology 2015-Dec

Role of Mitochondrial Calcium Uniporter in Early Brain Injury After Experimental Subarachnoid Hemorrhage.

Solo gli utenti registrati possono tradurre articoli
Entra registrati
Il collegamento viene salvato negli appunti
Huiying Yan
Dingding Zhang
Shuangying Hao
Kuanyu Li
Chun-Hua Hang

Parole chiave

Astratto

Previous studies have shown that mitochondrial Ca(2+) is undertaken by mitochondrial calcium uniporter (MCU), and its accumulation is associated with the development of many diseases. However, little was known about the role of MCU in early brain injury (EBI) after subarachnoid hemorrhage (SAH). MCU can be opened by spermine under a physiological condition and inhibited by ruthenium red (RR). Herein, we investigated the effects of RR and spermine to reveal the role of MCU in SAH animal model. The data obtained with biochemical and histological assays showed that mitochondrial Ca(2+) concentration was significantly increased in the temporal cortex of rats 1, 2, and 3 days after SAH, consistent with constant high levels of cellular Ca(2+) concentration. In agreement with the observation in the acute phase, SAH rats showed an obvious increase of reactive oxygen species (ROS) level and decrease of ATP production. Blockage of MCU prevented Ca(2+) accumulation, abated the level of oxidative stress, and improved the energy supply. Translocation of cytochrome c, increased cleaved caspase-3, and a large amount of apoptotic cells after SAH were reversed by RR administration. Surprisingly, exogenous spermine did not increase cellular Ca(2+) concentration, but lessened the Ca(2+) accumulation after SAH to benefit the rats. Taken together, our results demonstrated that blockage of MCU or prevention of Ca(2+) accumulation after SAH is essential in EBI after SAH. These findings suggest that MCU is considered to be a therapeutic target for patients suffering from SAH.

Unisciti alla nostra
pagina facebook

Il database di erbe medicinali più completo supportato dalla scienza

  • Funziona in 55 lingue
  • Cure a base di erbe sostenute dalla scienza
  • Riconoscimento delle erbe per immagine
  • Mappa GPS interattiva - tagga le erbe sul luogo (disponibile a breve)
  • Leggi le pubblicazioni scientifiche relative alla tua ricerca
  • Cerca le erbe medicinali in base ai loro effetti
  • Organizza i tuoi interessi e tieniti aggiornato sulle notizie di ricerca, sperimentazioni cliniche e brevetti

Digita un sintomo o una malattia e leggi le erbe che potrebbero aiutare, digita un'erba e osserva le malattie ei sintomi contro cui è usata.
* Tutte le informazioni si basano su ricerche scientifiche pubblicate

Google Play badgeApp Store badge