AI Article Synopsis
- Galanin has protective effects on cultured rat cortical astrocytes against oxidative stress triggered by HO, highlighting its potential neuroprotective role.
- The study shows that galanin treatment significantly reduces toxicity in astrocytes affected by oxidative stress, implicating the pERK1/2 signaling pathway in this protective mechanism.
- The expression levels of galanin receptors indicate that GalR2 is primarily responsible for mediating these protective effects, while galanin does not affect A1-type transformation in astrocytes.
Article Abstract
The neuropeptide galanin and its receptors have been found to have protective effects on neurons. However, the role of galanin on astrocytes is still unclear. The present study is aimed at investigating the effects of galanin on the viability of cultured rat cortical astrocytes after oxidative stress induced by HO and possible receptor and signaling mechanisms involved. Treatment of galanin had significant protective effects against HO-induced toxicity in the cultured cortical astrocytes. HO induced an upregulation of phosphorylated extracellular signal-related kinase1/2 (pERK1/2) in astrocytes, which was suppressed by coapplication of galanin, suggesting an involvement of the pERK1/2 signal pathway in the protective effects of galanin. GalR2 has higher expression levels than GalR1 and GalR3 in the cultured cortical astrocytes, and GalR2 agonist AR-M1896 mimicked galanin effects on the astrocytes, implying that galanin protective effects mainly mediated by GalR2. Meanwhile, galanin had no effect on the A1-type transformation of rat cortical astrocytes. All those results suggest that galanin protects rat cortical astrocytes from oxidative stress by suppressing HO-induced upregulation of pERK1/2, mainly through GalR2.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6556323 | PMC |
| http://dx.doi.org/10.1155/2019/2716028 | DOI Listing |
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