Jinglun Li
Northeast Forestry University
16 Papers
51 Citations
Jinglun Li is an academic researcher from Northeast Forestry University. The author has contributed to research in topics: Arsenic trioxide & Oxidative stress. The author has an hindex of 11, co-authored 15 publications.
Chat about Author
Papers
Copper (II) and/or arsenite-induced oxidative stress cascades apoptosis and autophagy in the skeletal muscles of chicken.
TL;DR: The present study showed that Cu and/or As induce oxidative damage in chicken skeletal muscles and discussed its mechanism in terms of apoptosis, autophagy, and mitochondrial dynamics, thus voicing concerns about poultry breeding areas cross-contaminated with Cu2+ and arsenite.
105
Synergistic effect of copper and arsenic upon oxidative stress, inflammation and autophagy alterations in brain tissues of Gallus gallus.
TL;DR: It is speculated that arsenic or copper could induce oxidative stress, inflammation and autophagy in chicken brains, and there may have a synergistic effect between copper and arsenic.
65
Copper or/and arsenic induce oxidative stress-cascaded, nuclear factor kappa B-dependent inflammation and immune imbalance, trigging heat shock response in the kidney of chicken.
TL;DR: Xing et al. as discussed by the authors showed that excessive amount of copper and inorganic arsenic coexists in drinking water in many regions, this is associated with high risk of nephropathy, defined as chronic structural and functional disorders of the kidney.
Copper or/and arsenic induces autophagy by oxidative stress-related PI3K/AKT/mTOR pathways and cascaded mitochondrial fission in chicken skeletal muscle
TL;DR: Together, the results showed that after Cu or/and As insult and accumulation, inhibited PI3K/AKT/mTOR pathway activated autophagy and disturbed mitochondrial dynamic, forming a positive feedback with redox disorder.
35
The inflammatory responses in Cu-mediated elemental imbalance is associated with mitochondrial fission and intrinsic apoptosis in Gallus gallus heart.
TL;DR: It is speculated that Cu-induced redistribution of trace elements contributed to inflammatory response and disrupted the mitochondrial network via fission and intrinsic apoptosis in the heart of chickens.
35