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

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.

Tributyltin-induced cell death is mediated by calpain in PC12 cells

2006 ◽  
Vol 27 (4) ◽  
pp. 587-593 ◽  
Author(s):  
Y NAKATSU ◽  
Y KOTAKE ◽  
S OHTA
Keyword(s):  
Cell Death ◽  
Pc12 Cells

Zn2+-induced ERK activation mediated by reactive oxygen species causes cell death in differentiated PC12 cells

2001 ◽  
Vol 78 (3) ◽  
pp. 600-610 ◽  
Author(s):  
Su Ryeon Seo ◽  
Seon Ah Chong ◽  
Syng-Ill Lee ◽  
Jee Young Sung ◽  
Young Soo Ahn ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Pc12 Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Erk Activation ◽  
Differentiated Pc12 Cells

scholarly journals Aurintricarboxylic acid rescues PC12 cells and sympathetic neurons from cell death caused by nerve growth factor deprivation: correlation with suppression of endonuclease activity.

1991 ◽  
Vol 115 (2) ◽  
pp. 461-471 ◽  
Author(s):  
A Batistatou ◽  
L A Greene
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Pc12 Cells ◽  
Sympathetic Neurons ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Endonuclease Activity ◽  
Term Survival ◽  
Serum Free

Past studies have shown that serum-free cultures of PC12 cells are a useful model system for studying the neuronal cell death which occurs after neurotrophic factor deprivation. In this experimental paradigm, nerve growth factor (NGF) rescues the cells from death. It is reported here that serum-deprived PC12 cells manifest an endonuclease activity that leads to internucleosomal cleavage of their cellular DNA. This activity is detected within 3 h of serum withdrawal and several hours before any morphological sign of cell degeneration or death. NGF and serum, which promote survival of the cells, inhibit the DNA fragmentation. Aurintricarboxylic acid (ATA), a general inhibitor of nucleases in vitro, suppresses the endonuclease activity and promotes long-term survival of PC12 cells in serum-free cultures. This effect appears to be independent of macromolecular synthesis. In addition, ATA promotes long-term survival of cultured sympathetic neurons after NGF withdrawal. ATA neither promotes nor maintains neurite outgrowth. It is hypothesized that the activation of an endogenous endonuclease could be responsible for neuronal cell death after neurotrophic factor deprivation and that growth factors could promote survival by leading to inhibition of constitutively present endonucleases.

NITRIC OXIDE-INDUCED CELL DEATH OF PC12 CELLS

1999 ◽  
Vol 27 (5) ◽  
pp. A146-A146
Author(s):  
A. Price ◽  
G.C. Brown
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Pc12 Cells

scholarly journals Nerve growth factor withdrawal-induced cell death in neuronal PC12 cells resembles that in sympathetic neurons.

1992 ◽  
Vol 119 (6) ◽  
pp. 1669-1680 ◽  
Author(s):  
P W Mesner ◽  
T R Winters ◽  
S H Green
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Programmed Cell Death ◽  
Pc12 Cells ◽  
Sympathetic Neurons ◽  
Nerve Growth ◽  
Neuronal Pc12 Cells ◽  
New Protein

Previous studies have shown that in neuronal cells the developmental phenomenon of programmed cell death is an active process, requiring synthesis of both RNA and protein. This presumably reflects a requirement for novel gene products to effect cell death. It is shown here that the death of nerve growth factor-deprived neuronal PC12 cells occurs at the same rate as that of rat sympathetic neurons and, like rat sympathetic neurons, involves new transcription and translation. In nerve growth factor-deprived neuronal PC12 cells, a decline in metabolic activity, assessed by uptake of [3H]2-deoxyglucose, precedes the decline in cell number, assessed by counts of trypan blue-excluding cells. Both declines are prevented by actinomycin D and anisomycin. In contrast, the death of nonneuronal (chromaffin-like) PC12 cells is not inhibited by transcription or translation inhibitors and thus does not require new protein synthesis. DNA fragmentation by internucleosomal cleavage does not appear to be a consistent or significant aspect of cell death in sympathetic neurons, neuronal PC12 cells, or nonneuronal PC12 cells, notwithstanding that the putative nuclease inhibitor aurintricarboxylic acid protects sympathetic neurons, as well as neuronal and nonneuronal PC12 cells, from death induced by trophic factor removal. Both phenotypic classes of PC12 cells respond to aurintricarboxylic acid with similar dose-response characteristics. Our results indicate that programmed cell death in neuronal PC12 cells, but not in nonneuronal PC12 cells, resembles programmed cell death in sympathetic neurons in significant mechanistic aspects: time course, role of new protein synthesis, and lack of a significant degree of DNA fragmentation.

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