scholarly journals Homocysteine and glutamate receptors in the neuronal dysfunction and cell death in levodopa therapy: Are B-complex vitamins and herbal medicine the panacea?

2013 ◽  
Vol 2 (3) ◽  
Author(s):  
B Ouattara ◽  
DM Angaman ◽  
A Coulibaly
2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Jia-Xin Ren ◽  
Chao Li ◽  
Xiu-Li Yan ◽  
Yang Qu ◽  
Yi Yang ◽  
...  

Oxidative stress is a key cause of ischemic stroke and an initiator of neuronal dysfunction and death, mainly through the overproduction of peroxides and the depletion of antioxidants. Ferroptosis/oxytosis is a unique, oxidative stress-induced cell death pathway characterized by lipid peroxidation and glutathione depletion. Both oxidative stress and ferroptosis/oxytosis have common molecular pathways. This review summarizes the possible targets and the mechanisms underlying the crosstalk between oxidative stress and ferroptosis/oxytosis in ischemic stroke. This knowledge might help to further understand the pathophysiology of ischemic stroke and open new perspectives for the treatment of ischemic stroke.


Proceedings ◽  
2019 ◽  
Vol 40 (1) ◽  
pp. 6
Author(s):  
Atalay ◽  
Imamoglu

Kynurenic Acid (KYNA) is a metabolite of tryptophan pathway and also an endogenous antagonist of glutamate receptors. Several studies indicated that glutamate antagonists have anti-proliferative potential. Moreover, subunits of the NMDA receptor which is one of the glutamate receptors have been shown to be found in human hepatocellular carcinoma cell line (HepG2). In this study, the antitumor effects of KYNA in HepG2 cells were investigated for the first time at the molecular level. The effects of KYNA on the viability of HepG2 cells were determined by MTT analyses. Effects of KYNA on mRNA transcriptions of apoptosis related genes Bax, Bcl-2 and Caspase-3 were analyzed by qRT-PCR. mRNA expression analysis revealed that the mRNA levels of effector Caspase-3 and pro-apoptotic Bax/Bcl-2 ratio were not increased in HepG2 cells treated with KYNA. In conclusion, our findings showed that KYNA does not exert its anti-proliferative effects on HepG2 cells through caspase-mediated apoptotic cell death, but it may perform this anti-proliferative effect through a different mechanism of death. Further studies are needed to find out potential cell death mechanisms that may play a role in anti-proliferative activity of KYNA on HepG2 cells.


Author(s):  
Xiuyu Wu ◽  
Ximin Hu ◽  
Qi Zhang ◽  
Fengxia Liu ◽  
Kun Xiong

: 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.


2002 ◽  
Vol 71 (4) ◽  
pp. 1544-1553 ◽  
Author(s):  
Terje Rootwelt ◽  
Michelle Dunn ◽  
Marc Yudkoff ◽  
Takayuki Itoh ◽  
Runar Almaas ◽  
...  

2003 ◽  
Vol 5 (30) ◽  
pp. 1-22 ◽  
Author(s):  
Michelle M. Aarts ◽  
Mark Arundine ◽  
Michael Tymianski

Brain injury following cerebral ischaemia (stroke) involves a complex combination of pathological processes, including excitotoxicity and inflammation leading to necrotic and apoptotic forms of cell death. At the cellular level, excitotoxicity is mediated by glutamate and its cognate receptors, resulting in increased intracellular calcium and free radical production, and eventual cell death. Recent evidence suggests that scaffolding molecules that associate with glutamate receptors at the postsynaptic density allow coupling of receptor activity to specific second messengers capable of mediating excitotoxicity. These findings have important implications in the search for effective neuroprotective therapies in treating stroke.


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