Abstract
Interleukin 10 (IL-10) is a synthetic inhibitor of human cytokines with immunomodulatory and anti-inflammatory effects. This study was designed to investigate the expression variation of IL-10 in the multiple sites including cortex, hippocampus, and lung tissues of neonatal hypoxic-ischemic (HI) rats and explore the crucial role of IL-10 in alleviating HI brain damage. In this study, neonatal Sprague-Dawley rats were subjected to the right common carotid artery ligation, followed by 2 h of hypoxia. The expression of IL-10 in the cortex, hippocampus, and lung tissues was measured with immunohistochemistry, real-time quantitative polymerase chain reaction (RT-qPCR), and western blot (WB). Immunofluorescence double staining was performed to observe the localization of IL-10 in neurons and astrocytes. Moreover, not-targeting and targeting IL-10 siRNA lentivirus vectors were injected into the rats of the negative control (NC) and IL-10 group, respectively, and the mRNA levels of B-cell lymphoma 2 (Bcl-2) and endoplasmic reticulum protein 29 (ERp29) were detected by RT-qPCR following IL-10 silence. The results demonstrated that the IL-10 expression was markedly increased after HI and IL-10 were colocalized with neurons and astrocytes which were badly injured by HI insult. In addition, Bcl-2 and ERp29 were remarkably decreased following IL-10 mRNA interference compared with the NC group. Our findings revealed that IL-10 exerted its antiapoptotic and neuroprotective effects by regulating the expression of Bcl-2 and ERp29, indicating that IL-10 may be a promising molecule target for HIE treatment.
Highlights
Hypoxic-ischemic encephalopathy (HIE) is one of the main threats to neonates in the perinatal period and a major contributor to global children morbidity and mortality [1, 2]
We found that Interleukin 10 (IL-10) was upregulated in the cortex, hippocampus, and lung tissues of neonatal HI rats accompanied by neurons and astrocyte damage, and IL-10 expressed in the neurons and astrocytes
The expression levels of B-cell lymphoma 2 (Bcl-2) and endoplasmic reticulum protein 29 (ERp29) were remarkably decreased following IL-10 mRNA interference (Figure 6). These results revealed that IL-10 might exert its antiapoptotic as well as a neuroprotective effect by regulating the expression of Bcl-2 and ERp29
Summary
Hypoxic-ischemic encephalopathy (HIE) is one of the main threats to neonates in the perinatal period and a major contributor to global children morbidity and mortality [1, 2]. It is estimated that about 1 to 8 per 1000 live births suffer hypoxic-ischemia (HI) in developed countries [3]. The death rates range from 10% to 60%, and 23% of survivors are obsessed with long-term neurodevelopmental sequelae [4]. Hypoxia usually causes such basic pathological changes as cerebral edema and neuronal necrosis, and ischemia mainly induces cerebral infarction and white matter softening [5]. Many methods were developed for HIE therapies with the advances in medical technology, such as hypothermia therapy [6, 7]; only about one in eight neonates can meet the eligibility criteria and benefit from the hypothermia therapy. Given limited benefit from hypothermia, investigations for more effective therapies are extremely urgent, and to explore the relative underlying mechanisms of HIE is fundamentally necessary
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