Circularly
polarized light (CPL) has considerable technological
potential, from quantum computing to bioimaging. To maximize the opportunity,
high performance photodetectors that can directly distinguish left-handed
and right-handed circularly polarized light are needed. Hybrid organic–inorganic
perovskites containing chiral organic ligands are an emerging candidate
for the active material in CPL photodetecting devices, but current
studies suggest there to be a trade-off between the ability to differentially
absorb CPL and photocurrent responsivity in chiral perovskites devices.
Here, we report a CPL detector based on quasi two-dimensional (quasi-2D)
chiral perovskite films. We find it is possible to generate materials
where the circular dichroism (CD) is comparable in both 2D and quasi-2D
films, while the responsivity of the photodetector improves for the
latter. Given this, we are able to showcase a CPL photodetector that
exhibits both a high dissymmetry factor of 0.15 and a high responsivity
of 15.7 A W
–1
. We believe our data further advocates
the potential of chiral perovskites in CPL-dependent photonic technologies.
Aim
Mitochondrial autophagy (mitophagy) clears damaged mitochondria and attenuates ischemic neuronal injury. Urolithin A (Uro‐A) activates mitophagy in mammal cells and Caenorhabditis elegans. We explored neuroprotection of Uro‐A against ischemic neuronal injury.
Methods
Mice were subjected to middle cerebral artery occlusion. The brain infarct and neurological deficit scores were measured. The N2a cells and primary cultured mice cortical neurons were subjected to oxygen‐glucose deprivation and reperfusion (OGD/R). Uro‐A was incubated during OGD/R, and cell injury was determined by MTT and LDH. Autophagosomes were visualized by transfecting mCherry‐microtubule‐associated protein 1 light chain 3 (LC3). The protein levels of LC3‐II, p62, Translocase Of Inner Mitochondrial Membrane 23 (TIMM23), and cytochrome c oxidase subunit 4 isoform 1 (COX4I1) were detected by Western blot. The ER stress markers, activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP), were determined by reverse transcription‐polymerase chain reaction (RT‐PCR).
Results
Urolithin A alleviated OGD/R‐induced injury in N2a cells and neurons and reduced ischemic brain injury in mice. Uro‐A reinforced ischemia‐induced autophagy. Furthermore, Uro‐A‐conferred protection was abolished by 3‐methyladenine, suggesting the requirement of autophagy for neuroprotection. However, mitophagy was not further activated by Uro‐A. Instead, Uro‐A attenuated OGD/R‐induced ER stress, which was abolished by 3‐methyladenosine. Additionally, neuroprotection was reversed by ER stress inducer.
Conclusion
Urolithin A protected against ischemic neuronal injury by reinforcing autophagy rather than mitophagy. Autophagy activation by Uro‐A attenuated ischemic neuronal death by suppressing ER stress.
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