(S)-ZJM-289, a nitric oxide-releasing derivative of 3-n-butylphthalide, protects against ischemic neuronal injury by attenuating mitochondrial dysfunction and associated cell death

2012 ◽  
Vol 60 (2) ◽  
pp. 134-144 ◽  
Author(s):  
Qian Zhao ◽  
Chao Zhang ◽  
Xuliang Wang ◽  
Li Chen ◽  
Hui Ji ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Mitochondrial Dysfunction ◽  
Neuronal Injury ◽  
Nitric Oxide Releasing ◽  
Ischemic Neuronal Injury

Nitric oxide-induced cell death in developing oligodendrocytes is associated with mitochondrial dysfunction and apoptosis-inducing factor translocation

2004 ◽  
Vol 20 (7) ◽  
pp. 1713-1726 ◽  
Author(s):  
Olivier Baud ◽  
Jianrong Li ◽  
Yumin Zhang ◽  
Rachael L. Neve ◽  
Joseph J. Volpe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Mitochondrial Dysfunction ◽  
Apoptosis Inducing Factor

scholarly journals Somatic autophagy of axonal mitochondria in ischemic neurons

2019 ◽  
Vol 218 (6) ◽  
pp. 1891-1907 ◽  
Author(s):  
Yanrong Zheng ◽  
Xiangnan Zhang ◽  
Xiaoli Wu ◽  
Lei Jiang ◽  
Anil Ahsan ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Neuronal Injury ◽  
Glucose Deprivation ◽  
Retrograde Transport ◽  
Direct Link ◽  
Mitochondrial Content ◽  
Oxygen And Glucose Deprivation ◽  
Mitochondrial Movement ◽  
Mitochondrial Motility ◽  
Ischemic Neuronal Injury

Mitophagy protects against ischemic neuronal injury by eliminating damaged mitochondria, but it is unclear how mitochondria in distal axons are cleared. We find that oxygen and glucose deprivation-reperfusion reduces mitochondrial content in both cell bodies and axons. Axonal mitochondria elimination was not abolished in Atg7fl/fl;nes-Cre neurons, suggesting the absence of direct mitophagy in axons. Instead, axonal mitochondria were enwrapped by autophagosomes in soma and axon-derived mitochondria prioritized for elimination by autophagy. Intriguingly, axonal mitochondria showed prompt loss of anterograde motility but increased retrograde movement upon reperfusion. Anchoring of axonal mitochondria by syntaphilin blocked neuronal mitophagy and aggravated injury. Conversely, induced binding of mitochondria to dynein reinforced retrograde transport and enhanced mitophagy to prevent mitochondrial dysfunction and attenuate neuronal injury. Therefore, we reveal somatic autophagy of axonal mitochondria in ischemic neurons and establish a direct link of retrograde mitochondrial movement with mitophagy. Our findings may provide a new concept for reducing ischemic neuronal injury by correcting mitochondrial motility.

Regulatory Role Of Chinese Herbal Medicine In Regulated Neuronal Death

2020 ◽  
Vol 19 ◽  
Author(s):  
Xiuyu Wu ◽  
Ximin Hu ◽  
Qi Zhang ◽  
Fengxia Liu ◽  
Kun Xiong
Keyword(s):  
Cell Death ◽  
Herbal Medicine ◽  
Chinese Herbal Medicine ◽  
Synergistic Effects ◽  
Neuronal Injury ◽  
Therapeutic Effects ◽  
Chinese Herbal ◽  
Regulated Cell Death ◽  
Nitrative Stress ◽  
Ischemic Neuronal Injury

: Ischemic neuronal injury results from a complex series of pathophysiological events, including oxidative, excitotoxicity, inflammation and nitrative stress. Consequently, many of these events can induce cell death, including necrosis (unregulated cell death) and apoptosis (a type of regulated cell death). These are long-established paradigms to which newly discovered regulated cell death processes have been added, such as necroptosis (a regulated form of necrosis) and autophagy-dependent cell death. Moreover, many researchers have targeted products associated with Chinese herbal medicine at regulated pathways for the treatment of ischemic neuronal injury. In East Asia, these drugs have been known for centuries to protect and improve the nervous system. Herbal extracts, especially those used in Chinese herbal medicine, have emerged as new pharmaceuticals for the treatment of ischemic neuronal injury. Here, we review the evidence from preclinical studies investigating the neuroprotective properties and therapeutic application of Chinese herbal medicines (Chinese herbal monomer, extract, and medicinal compounds) and highlight the potential mechanisms underlying their therapeutic effects via targeting different regulated cell death pathways. Notably, many herbs have been shown to target multiple mechanisms of regulated cell death and, in combination, may exert synergistic effects on signaling pathways, thereby attenuating multiple aspects of ischemic pathology. In this review, we summarize a general regulated pathway of cell death as a target for novel natural herbal regimens against ischemic neuronal injury.

scholarly journals Crosstalk between Nitric Oxide and Zinc Pathways to Neuronal Cell Death Involving Mitochondrial Dysfunction and p38-Activated K+ Channels

Neuron ◽  
2004 ◽  
Vol 41 (3) ◽  
pp. 351-365 ◽  
Author(s):  
Ella Bossy-Wetzel ◽  
Maria V Talantova ◽  
Wilson D Lee ◽  
Marion N Schölzke ◽  
Anne Harrop ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Mitochondrial Dysfunction ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
K Channels

Minocycline attenuates both OGD-induced HMGB1 release and HMGB1-induced cell death in ischemic neuronal injury in PC12 cells

2009 ◽  
Vol 385 (2) ◽  
pp. 132-136 ◽  
Author(s):  
Kiyoshi Kikuchi ◽  
Ko-ichi Kawahara ◽  
Kamal Krishna Biswas ◽  
Takashi Ito ◽  
Salunya Tancharoen ◽  
...  
Keyword(s):  
Cell Death ◽  
Pc12 Cells ◽  
Neuronal Injury ◽  
Ischemic Neuronal Injury
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