Effect of Dexmedetomidine on The Neuroglobin Expression in Elderly Patients With Minimally Invasive Coronary Artery Bypass Graft Surgery.

BACKGROUND: To study the effect of dexmedetomidine (Dex) on the expression of Neuroglobin (Ngb) and postoperative cognitive function in elderly patients undergoing minimally invasive coronary artery bypass surgery. METHODS: Forty patients, who underwent elective minimally invasive off-pump coronary artery bypass grafting in our hospital from January 2018 to December 2019, were randomly divided into the Dex group (N = 20) and control group (N = 20). Venous blood samples were taken to determine the expression level of Ngb in both groups. Mini mental status examination (MMSE) was used to detect the cognitive function of patients. RESULTS: The expression level of Ngb in the Dex group was significantly higher than that in the control group at 6h after one-lung ventilation and postoperative 24h (P < .01). The MMSE score of the Dex group was significantly higher than the control group at postoperative 7 days and postoperative 30 days (P < .01). Although with no statistical significance, the MMSE score of the Dex group was higher than the control group at postoperative 90 days (P > .05). The incidence of postoperative cognitive dysfunction (POCD) in the Dex group was significantly lower than that in the control group at postoperative 7 days and postoperative 30 days (P < .05). CONCLUSION: Dex used in elderly patients undergoing minimally invasive coronary artery bypass graft surgery can effectively increase the expression level of Ngb and reduce the incidence of POCD.

Neuroglobin protects offspring rats from neuronal damage induced by sevoflurane exposure to pregnant rats by inhibiting endogenous apoptosis.

As a general anesthesia drug, sevoflurane has been found to be potentially neurotoxic to the developing brain. Neuroglobin (Ngb) is a novel oxygen-carrying globulin that has been demonstrated to have neuroprotective effects in a variety of central nervous system disorders. However, it is unclear whether Ngb has a protective effect on nerve damage caused by sevoflurane. Therefore, this study was designed to investigate the effect and related mechanisms of Ngb on neural injury induced by sevoflurane. Pregnant rats on gestational day 20 (G20) were exposed to 3.5% sevoflurane for two hours, which led to an increase of Ngb on the 0-1st day after birth and decreased significantly on the 3rd day, while Cytochrome c increased from the 1 st day until the 7th day of offspring rats. Meanwhile, sevoflurane reduced Bcl-2 and Hif-1αand increased Bax and cleaved-caspase 3 in the third day after birth. Hemin inhibits endogenous apoptosis by increasing Ngb and Hif-1α. And increased Ngb improved the damage of long-term learning and memory induced by sevoflurane and increased the number of neurons in the hippocampus. We concluded that Ngb can improve the neuronal injury induced by sevoflurane exposure by inhibiting apoptosis and increasing the number of neurons. And this protective effect of Ngb may be related to Hif-1α signaling pathway. This finding may provide a novel therapeutic approach for sevoflurane -induced nerve damage.

Recombinant neuroglobin ameliorates early brain injury after subarachnoid hemorrhage via inhibiting the activation of mitochondria apoptotic pathway.

Neuroglobin (Ngb) overexpression is considered as an intrinsic neuroprotective response. Therefore, exogenous Ngb increased in brain tissues has become a promising therapeutic strategy for neurological diseases. Previous studies demonstrated that transactivator of transcription (TAT) protein transduction domain was able to mediate synthetic Ngb entrance into neurons, and then protected brain from hypoxia-ischemic injury. However, the role of recombinant Ngb on early brain injury following subarachnoid hemorrhage (SAH) has not been elucidated. The objectives of this study were to investigate the expression of endogenous Ngb in brain using a rabbit model of SAH, and to verify whether TAT-Ngb fusion protein could be delivered into brain parenchyma, as well as to explore the neuroprotective effect of Ngb and its possible mechanisms. We found that Ngb expressions were up regulated in the transcript and protein levels in a similar time dependent manner after SAH as compared to the sham group. Moreover, TAT-Ngb fusion protein was successfully generated and transferred into brain neurons. Compared with the saline- and Ngb-treated group, neuronal viabilities and neurological outcomes were significantly improved 72 h post-SAH in the TAT-Ngb-treated group. Likewise, anti-apoptotic Bcl-2 protein was also elevated obviously. Conversely, pro-apoptotic factors including caspase 3, caspase 9 and Bax were greatly decreased after TAT-Ngb treatment. Our results suggest that Ngb plays a neuroprotective effect in rabbits suffering from SAH possibly through inhibiting the SAH-induced activation of mitochondria apoptotic pathway. Furthermore, TAT-mediated Ngb delivery into brain may be a promising therapeutic approach.