Total flavones of Rhododendron simsii Planch flower protect rat hippocampal neuron from hypoxia-reoxygenation injury via activation of BKCa channel

Abstract

Objectives To study the effects of total flavones of Rhododendra simsii Planch flower (TFR) on hypoxia/reoxygenation (H/R) injury in rat hippocampal neurons and its underlying mechanism. Method Model of H/R was established in newborn rat primary cultured hippocampal neuron. Lactate dehydrogenase (LDH) and neuron‐specific enolase (NSE) activity as well as malondialdehyde (MDA) content in cultured supernatants of the neurons were examined. Methyl thiazolyl tetrazolium assay and Hoechst33258 staining were, respectively, used to detect cell viability and apoptosis of neurons. Protein expression and current of BKCa channel were assessed by using Western blotting and whole‐cell patch‐clamp methods, respectively. Key findings In the ranges of 3.7–300 mg/l, TFR significantly inhibited H/R‐induced decrease of neuronal viability and increases of LDH, NSE and MDA in the supernatants as well as apoptosis; TFR 33.3, 100 and 300 mg/l markedly increased current of BKCa channel rather than the BKCa channel protein expression in the neurons. Conclusions Total flavones of R. simsii Planch flower had a protective effect against H/R injury in rat hippocampal neuron, and activation of BKCa channel may contribute to the neuroprotection.

Protection against Hypoxia-Reoxygenation Injury of Hippocampal Neurons by H2S via Promoting Phosphorylation of ROCK2 at Tyr722 in Rat Model

“…Therefore, it could be concluded that phosphorylation of ROCK 2 at Tyr722 also mediates protective effect of H 2 S against H/R injury in RHNs. It was well-known that inhibition of the RhoA-ROCK signaling pathway protects cerebral ischemia-reperfusion injury [ 34 , 35 ]. Combined with the above-mentioned that H 2 S promotes the phosphorylation of ROCK 2 at Tyr722 to inhibit ROCK 2 activity in RHNs, our results demonstrated that H 2 S protects RHNs from H/R injury through promoting phosphorylation of ROCK 2 at Tyr722 to inhibit ROCK 2 activity.…”

Endothelium‐derived hydrogen sulfide acts as a hyperpolarizing factor and exerts neuroprotective effects via activation of large‐conductance Ca2+‐activated K+ channels

“…For OGD/R (Chen et al, 2013), hippocampal neurons were subjected to 4 h of hypoxia induced by replacing culture medium with glucose‐free D‐Hank's solution (in mg·L −1 : 8000 NaCl, 400 KCl, 510 Na 2 HPO 4 ·12H 2 O, 60 KH 2 PO 4 and 350 NaHCO 3 , pH 7.2–7.4) under the condition of 94% N 2 , 5% CO 2 and 1% O 2 and 24 h of reoxygenation induced by replacing the glucose‐free D‐Hank's solution with normal culture medium and being incubated under normal condition. In NaHS or the other drug treatment groups, cells were respectively treated with NaHS (1 × 10 −6 M) (Wen et al, 2018), iberiotoxin (100 nM) (Guo et al, 2020), BMS‐191011 (10 μM) (Levin et al, 2016), NNC 55‐0396 (100 μM) (Angstadt et al, 2017) or verapamil (100 μM) (Tang et al, 2016) before and during OGD/R.…”

Metabolic Impact of Flavonoids Consumption in Obesity: From Central to Peripheral

“…Luteolin administration alleviated neuroinflammation, oxidative stress and neuronal insulin resistance as well as improved the Morris water maze (MWM) and step-through task and increased the levels of BDNF [ 373 ]. Other effects of flavones described recently are anxiolytic-like activity [ 374 ], neuroprotection against gamma-radiation [ 375 ] treatment of glioblastoma [ 376 ], amelioration of the hypoxia-reoxygenation injury [ 377 ] or inhibition of the neuroinflammation caused by LPS [ 378 ].…”