CTRP6(C1q/Tumor Necrosis Factor (TNF)-related protein-6) alleviated the sevoflurane induced injury of mice central nervous system by promoting the expression of p-Akt (phosphorylated Akt)

ABSTRACT

Postoperative cognitive impairment and nervous system damage caused by anesthetics seriously affect patient’s postoperative recovery. Recent study has revealed that CTRP6 could alleviate apoptosis, inflammation and oxidative stress of nerve cells, thereby relieving nervous system damage induced by cerebral ischemia reperfusion. However, whether CTRP6 could relieve sevoflurane induced central nervous system injury is unclear. We stimulated C57BL/6 mice with sevoflurane and injected CTRP6 overexpression adenovirus vector. Next, H&E staining and TUNEL assays were performed to examine the effect of CTRP6 on sevoflurane induced injury of central nervous system. Finally, we isolated primary nerve cells of hippocampus. Flow cytometry and commercial kits were used for the detection of apoptosis and ROS levels of these cells. Western blotting was used for the detection of the expression level of p-Akt in central nervous tissues and primary cells. Results showed that sevoflurane induced injury and apoptosis of central nervous tissues. Overexpression of CTRP6 relieved apoptosis and injury of these tissues. CTRP6 inhibited the expression of cleaved caspase-3 and cleaved PARP in these tissues. Sevoflurane promoted apoptosis of primary cells and enhanced the expression of ROS and MDA in these cells. Overexpression of CTRP6 alleviated apoptosis and suppressed production of ROS and MDA in these cells. In addition, CTRP6 also enhanced the expression of p-Akt in primary cells. Taken together, our results suggested that CTRP6 relieved sevoflurane induced injury of central nervous tissues by promoting the expression of p-Akt. Therefore, the targeted drug of CTRP6 should be explored for the remission of these symptoms.

KEYWORDS:

• Sevoflurane
• central nervous system injury
• apoptosis
• CTRP6
• p-Akt

Highlight

1. Overexpression of CTRP6 alleviated the sevoflurane induced injury of central nervous tissues

2. Overexpression of CTRP6 relieved the sevoflurane induced apoptosis of central nervous tissues

3. Overexpression of CTRP6 rescued the memory and learning ability of mice

4. CTRP6 protected primary cells of nerve tissue from sevoflurane induced apoptosis

5. CTRP6 relieved the sevoflurane induced oxidative stress of primary cells of nerve tissue

Abbreviations

POCD: Postoperative cognitive dysfunction

TNF: Tumor Necrosis Factor

CTRP6: C1q/Tumor Necrosis Factor (TNF)-related Protein-6

Disclosure statement

No potential conflict of interest was reported by the author(s).

Ethics approval

Ethical approval was obtained from the Ethics Committee of The Second Hospital， University to South China Hengyang Cty.

Availability of data and materials

All data generated or analyzed during this study are included in this published article.

Code availability

Not applicable.

Authors’ contributions

Zhiwen Liu and Bin Yang designed the study, supervised data collection, Zhiwen Liu analyzed the data, interpreted the data, Bin Yang prepared the manuscript for publication and reviewed the draft of the manuscript. All authors have read and approved the manuscript.

Additional information

Funding

The authors have no funding to report.