scispace - formally typeset
M

Mei-Jie Jou

Researcher at Chang Gung University

Publications -  24
Citations -  2154

Mei-Jie Jou is an academic researcher from Chang Gung University. The author has contributed to research in topics: Mitochondrion & Mitochondrial permeability transition pore. The author has an hindex of 19, co-authored 24 publications receiving 1953 citations.

Papers
More filters
Journal ArticleDOI

Oxidative stress caused by mitochondrial calcium overload

TL;DR: The reciprocal interactions between Ca2+ induced ROS increase and ROS modulatedCa2+ upsurge may cause a feedforward, self‐amplified loop createing cellular damage far beyond direct Ca2- induced damage.
Journal ArticleDOI

Visualization of the antioxidative effects of melatonin at the mitochondrial level during oxidative stress-induced apoptosis of rat brain astrocytes

TL;DR: The powerful mitochondrial protection provided by melatonin reinforces its therapeutic potential to combat a variety of oxidative stress‐induced mitochondrial dysfunctions as well as mitochondria‐mediated apoptosis in various diseases.
Journal ArticleDOI

Melatonin protects against common deletion of mitochondrial DNA-augmented mitochondrial oxidative stress and apoptosis.

TL;DR: Melatonin significantly prevents CD‐augmented mROS formation under basal conditions as well as at early time‐points upon secondary oxidative stress induced by H2O2 exposure, and may serve as a therapeutic drug to benefit many clinical conditions that involve malfunction of the mitochondria.
Journal ArticleDOI

Visualization of melatonin’s multiple mitochondrial levels of protection against mitochondrial Ca2+-mediated permeability transition and beyond in rat brain astrocytes

TL;DR: These multiple mitochondrial layers of protection provided by melatonin against mCa2+‐and/or mROS‐mediated apoptosis in astrocytes may be crucial for future therapeutic prevention and treatment of astroCyte‐mediated neurodegenerative diseases in the CNS.
Journal ArticleDOI

Involvement of p42/p44 MAPK, p38 MAPK, JNK and nuclear factor-kappa B in interleukin-1beta-induced matrix metalloproteinase-9 expression in rat brain astrocytes.

TL;DR: Results suggest that in RBA‐1 cells, activation of p42/p44 MAPK, p38, JNK and NF‐κB pathways is essential for IL‐1β‐induced MMP‐9 gene expression via transcription and translation processes.