sodium-nitrite and Brain-Injuries

Subarachnoid haemorrhage (SAH) is associated with long-term disability, serious reduction in quality of life and significant mortality. Early brain injury (EBI) refers to the pathological changes in cerebral metabolism and blood flow that happen in the first few days after ictus and may lead on to delayed cerebral ischaemia (DCI). A disruption of the nitric oxide (NO) pathway is hypothesised as a key mechanism underlying EBI. A decrease in the alpha-delta power ratio (ADR) of the electroencephalogram has been related to cerebral ischaemia. In an experimental medicine study, we tested the hypothesis that intravenous sodium nitrite, an NO donor, would lead to increases in ADR. We studied 33 patients with acute aneurysmal SAH in the EBI phase. Participants were randomised to either sodium nitrite or saline infusion for 1 h. EEG measurements were taken before the start of and during the infusion. Twenty-eight patients did not develop DCI and five patients developed DCI. In the patients who did not develop DCI, we found an increase in ADR during sodium nitrite versus saline infusion. In the five patients who developed DCI, we did not observe a consistent pattern of ADR changes. We suggest that ADR power changes in response to nitrite infusion reflect a NO-mediated reduction in cerebral ischaemia and increase in perfusion, adding further evidence to the role of the NO pathway in EBI after SAH. Our findings provide the basis for future clinical trials employing NO donors after SAH.

Topics: Biomarkers; Brain Injuries; Brain Ischemia; Cerebral Infarction; Electroencephalography; Humans; Quality of Life; Sodium Nitrite; Subarachnoid Hemorrhage

Food safety and nutrition during pregnancy are important concerns related to fetal brain development. In the present study, we aimed to explore the effects of omega-3 polyunsaturated fatty acids (PUFA ω-3) on exogenous sodium nitrite intervention-induced fetal brain injury in pregnant rats.. During pregnancy, rats were exposed to water containing sodium nitrite (0.05%, 0.15%, and 0.25%) to establish a fetal rat brain injury model. Inflammatory factors and oxidative stress levels were detected using enzyme-linked immunosorbent assay (ELISA) or flow cytometry. Subsequently, animals were divided into three groups: control, model, and 4% PUFA ω-3. Pregnancy outcomes were measured and recorded. Hematoxylin-eosin (H&E) staining and immunohistochemistry (IHC) were utilized to observe brain injury. ELISA, quantitative real-time PCR (qRT-PCR), western blot, flow cytometry, and transmission electron microscopy (TEM) were adopted to measure the levels of inflammatory factors, the NRF1/HMOX1 signaling pathway, and mitochondrial and oxidative stress damage.. With the increase of sodium nitrite concentration, the inflammatory factors and oxidative stress levels increased. Therefore, the high dose group was set as the model group for the following experiments. After PUFA ω-3 treatment, the fetal survival ratio, average body weight, and brain weight were elevated. The cells in the PUFA ω-3 group were more closely arranged and more round than the model. PUFA ω-3 treatment relieved inflammatory factors, oxidative stress levels, and mitochondria damage while increasing the indicators related to brain injury and NRF1/HMOX1 levels.. Sodium nitrite exposure during pregnancy could cause brain damage in fetal rats. PUFA ω-3 might help alleviate brain inflammation, oxidative stress, and mitochondrial damage, possibly through the NRF1/HMOX1 signaling pathway. In conclusion, appropriately reducing sodium nitrite exposure and increasing PUFA omega-3 intake during pregnancy may benefit fetal brain development. These findings could further our understanding of nutrition and health during pregnancy.

Topics: Animals; Brain Injuries; Dietary Supplements; Encephalitis; Fatty Acids, Omega-3; Female; Inflammation; Pregnancy; Rats; Sodium Nitrite

The brain insulin receptor and ERK I/II are known to play an important role in memory formation and neuroprotection. A series of experiments was designed to explore if Liriopsis tuber (LT) extracts could exhibit neuroprotection and memory enhancing actions. LT was extracted with 70% methanol and subsequently fractionated into chloroform (fraction C), chloroform/methanol-(3:1) (fraction CM), methanol-soluble (fraction M) and methanol-insoluble, water-soluble fractions (fraction A). The LT fractions (T, C, M, A) significantly inhibited the cortical depolarization induced by AMPA in cortical slices of rats. In addition, these fractions were also effective in promoting memory in the passive avoidance test in mice. To gain insight into the mechanism of memory enhancing effects by Liriopsis tuber extracts, the activities of hippocampal insulin receptors and ERK I/II were tested in rats. Extract of LT (T) dramatically stimulated tyrosine phosphorylation of the insulin receptor, while fraction C of LT also significantly stimulated the same. In addition, ERK I/II were stimulated and cholinesterase activities were inhibited by fractions T, C, M and A in the rat hippocampus. These results suggest that Liriopsis tuber extracts may exert neuroprotection and memory enhancing effects via activation of the insulin receptor and ERK I/II as well as inhibiting cholinesterase.

Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Avoidance Learning; Brain Injuries; Electrophysiology; Hippocampus; Hypoxia; Magnoliopsida; Male; Memory; Mice; Mice, Inbred ICR; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; Neuroprotective Agents; Phosphorylation; Phytotherapy; Plant Extracts; Plant Tubers; Rats; Rats, Sprague-Dawley; Receptor, Insulin; Sodium Nitrite