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NLRC5 protects neurons from oxygen-glucose deprivation-induced injury through activating the Nrf2/HO-1 pathway
Linlin Li1, Ming Yu1, Hongbo Pang1
1The Third Ward of Nerve Center, Suining Central Hospital, Suining, China.
Abstract:
NLRC5 is a member of the Nod-like receptor (NLR) family that has been found to be associated with the hepatic ischemia/reperfusion (I/R) injury. However, the role of NLRC5 in cerebral I/R has not been fully understood. The aim of the current study was to evaluate the effects of NLRC5 on primary hippocampal neuronal cells exposed to oxygen-glucose deprivation/reperfusion (OGD/R). Our results showed that the mRNA and protein levels of NLRC5 were significantly decreased in OGD/R-induced neurons. Overexpression of NLRC5 caused significant increase in cell viability, as well as decrease in ROS level. The bax expression was significantly decreased, while bcl-2 expression was increased in NLRC5-overexpressing neurons. Furthermore, increased nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression levels were observed in neurons transfected with pcDNA3.0-NLRC5. The mRNA levels of HO-1, NAD(P)H:quinone oxidoreductase 1 (NQO-1) and glutathione peroxidase 3 (GPx-3) were induced by NLRC5 overexpression in OGD/R-induced hippocampal neurons. Additionally, inhibition of Nrf2/HO-1 pathway abolished the protective effect of NLRC5 on cerebral I/R injury. In conclusion, these results indicated that NLRC5 protected hippocampal neurons from OGD/R-induced injury. The protective effects of NLRC5 were mediated by the Nrf2/HO-1 pathway. Thus, NLRC5 might serve as an effective target for the treatment of cerebral I/R injury.
Insights
NLRC5 protects hippocampal neurons from cerebral ischemia/reperfusion (I/R) injury by activating the Nrf2/HO-1 pathway. This finding suggests NLRC5 as a potential therapeutic target for I/R-related brain damage.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- NLRC5, a Nod-like receptor, is linked to liver ischemia/reperfusion (I/R) injury.
- Its role in cerebral I/R injury remains unclear.
- Investigating NLRC5 in primary hippocampal neurons under oxygen-glucose deprivation/reperfusion (OGD/R) is crucial.
Purpose of the Study:
- To investigate the role of NLRC5 in cerebral I/R injury.
- To determine the effects of NLRC5 on primary hippocampal neuronal cells exposed to OGD/R.
- To elucidate the underlying molecular mechanisms of NLRC5-mediated protection.
Main Methods:
- Primary hippocampal neuronal cells were subjected to OGD/R.
- NLRC5 expression was modulated (overexpression).
- Cell viability, reactive oxygen species (ROS) levels, apoptosis-related proteins (Bax, Bcl-2), and the Nrf2/HO-1 pathway were assessed.
Main Results:
- NLRC5 mRNA and protein levels decreased in OGD/R neurons.
- NLRC5 overexpression increased cell viability and reduced ROS.
- NLRC5 upregulated Nrf2, HO-1, NQO-1, and GPx-3, while decreasing Bax and increasing Bcl-2.
- Inhibition of the Nrf2/HO-1 pathway abrogated NLRC5's protective effects.
Conclusions:
- NLRC5 confers protection to hippocampal neurons against OGD/R-induced injury.
- The protective mechanism involves the activation of the Nrf2/HO-1 pathway.
- NLRC5 represents a promising therapeutic target for cerebral I/R injury.
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