Sevoflurane alleviates hypoxic-ischemic encephalopathy by regulating G9a expression. PC-12 (well differentiated) cells

"Bioengineered" IF: 3.

The mechanism of sevoflurane post-treatment alleviating hypoxic-ischemic encephalopathy by affecting histone methyltransferase G9a in rats

Learning is boundless in the ocean, and we make a boat with literature.

Today, let's take a look at a literature on the research of hypoxic-ischemic encephalopathy.

First of all, what is hypoxic-ischemic encephalopathy?

Hypoxic ischemic encephalopathy (HIE) is an important cause of morbidity and mortality in term neonates, mainly resulting in neuronal and cerebral white matter damage, which may further affect infant nervous system development, cognitive impairment and even death

Hypothermia is the only officially approved treatment recommendation for HIE, but it has limited effect on preventing neurological damage, so HIE can be tricky when it occurs

According to previous reports, sevoflurane (SF) can reduce nervous system damage, cerebral infarction and neuronal apoptosis, and alleviate HIE.

In order to verify this conjecture, the author designed two parts of animal in vivo experiments and in vitro experiments

In vivo experiments, the HIE model was first established in SD rats, and then the Sham group, the HIE group, the HIE+SF treatment group, the HIE+SF+AAV-G9a overexpression group, and the HIE+SF+AAV-NC control group were subjected to rat behavioral studies.

At the same time, the HIE+SF+AAV-G9a overexpression group and the HIE+SF+AAV-NC control group were subjected to behavioral experiments, HE staining of brain tissue, and TUNEL staining of the hippocampus.

The following only shows the experimental results of some animal models (the experimental results have been re-adjusted and are not described in the original text):

 

a: HE staining results of rat brain tissue, showing that the arrangement and state of nerve cells in the HIE group were abnormal, while the HIE+SF group and the Sham group were normal;

 

b: Nissl staining results of rat brain tissue, showing that the nerve cells in the HIE group were significantly reduced, while the HIE+SF group and the Sham group were normal;

 

c: TUNEL staining results of the hippocampus tissue, showing that the apoptosis of neurons in the HIE group was significantly increased, and the HIE+SF group and the Sham group were normal;

 

d: The results of ELISA and WB detection in brain tissue showed that the expression of G9a was increased in the HIE group, and the expression of BDNF and NGF was decreased;

The results of HIE+SF+AAV-G9a overexpression group and HIE+SF+AAV-NC control group were similar to the above HIE group and Sham group.

e: Cell experiments showed that the expression of G9a was increased in the OGD group, but decreased in the OGD+SF group, and the cells overexpressing G9a were also significantly increased;

 

f: Cell experiments showed that the same as the results of animal model experiments, the expression of BDNF in the OGD group was decreased, the expression in the OGD+SF group was increased, and the cells overexpressing G9a were also significantly decreased;

 

Conclusion: The above studies show that the increase of G9a can induce the symptoms of HIE, and SF can significantly relieve the symptoms of HIE, reduce the expression level of G9a, increase the expression of BDNF, reduce nerve damage, and improve the memory ability of rats

Well, today's literature is simply parsed here.

The PC-12 well-differentiated (Sunncell Biotechnology Inc, SNL-124) cells used in the literature are derived from transplantable male rat adrenal pheochromocytoma.

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