Role of immunoglobulin in neuronal apoptosis in a neonatal rat model of hypoxic ischemic brain injury

Abstract

The objective of the present study was to evaluate the neuroprotective effects of immunoglobulin (Ig) in a neonatal hypoxic ischemic (HI) rat model. Seven-day-old rat pups were randomly assigned to control, hypoxia and hypoxia + Ig groups. The rats in the hypoxia +Ig group were intraperitoneally administered 1 g/kg Ig once, immediately after hypoxia. Saline was administered to the rats in the hypoxia group at the same time point. Eight rats from each of the Ig + hypoxia and hypoxia groups were sacrificed by decapitation 4 and 24 h following the administration of Ig or saline. The rats of the control group were sacrificed at the 4 h time-point. Caspase-3 activity, as well as IL-1β, IL-6 and TNF-α mRNA expression levels, were studied in the left ischemic hemispheres. Induction of cerebral ischemia increased the TNF-α, IL-6 and IL-1β mRNA expression levels significantly at 4 and 24 h in the left ischemic hemispheres in the hypoxia group compared with those in the control group. The systemic administration of Ig following HI encephalopathy significantly reduced the TNF-α, IL-6 and IL-1β mRNA expression levels in the ischemic tissue in the Ig + hypoxia group compared with those in the hypoxia group. In the hypoxia group, caspase-3 activity in the left half of the brain was found to be significantly increased compared with that in the control group. Caspase-3 activity in the Ig + hypoxia group was significantly lower than that in the hypoxia group. The observations of the present study indicate that Ig administration may be an efficient treatment approach for reducing cerebral apoptosis associated with hypoxic ischemia.

Regulatory effect of Bcl-2 in ultraviolet radiation-induced apoptosis of the mouse crystalline lens

“…In addition, UV radiation may lead to DNA damage, including the formation of base-free loci and pyrimidine dimers, which severely affect DNA duplication and transcription. Subsequently, DNA damage may be repaired to enable the cells to survive continuously, while programed cell death or apoptosis may be utilized to eliminate the defective individual cells; thus, maintaining the structural and functional completeness of the crystalline lens (7,8). However, the intrinsic physiological functions of the crystalline lens are likely to be affected, resulting in a series of pathological changes if apoptosis occurs to a number of cells, or if the apoptotic cells can not be offset by proliferation (9,10).…”

Midazolam Inhibits the Apoptosis of Astrocytes Induced by Oxygen Glucose Deprivation via Targeting JAK2-STAT3 Signaling Pathway

“…Apoptosis, also called programmed cell death, is a pathway of cell death distinguished by such features as chromatin and cytoplasmic condensation and nuclear fragmentation, which has been implicated in several disorders of the central nervous system including ischemic brain injury [10], Alzheimer's disease [11], and multiple sclerosis [12]. But the focus of most these reported studies has been on neuronal apoptosis.…”

Anti-apoptotic and Immunomodulatory Effect of CB2 Agonist, JWH133, in a Neonatal Rat Model of Hypoxic-Ischemic Encephalopathy

“…Tumor necrosis factor alpha (TNFα) levels peak at 4-6 h following hypoxic ischemic injury (11,18) with some elevation at 24 h (18). In our study, TNFα was significantly elevated at 24 h in the HIE group.…”