Multi-omics reveal neuroprotection of Acer truncatum Bunge Seed extract on hypoxic-ischemia encephalopathy rats under high-altitude.

Hypoxic-ischemic encephalopathy (HIE) at high-altitudes leads to neonatal mortality and long-term neurological complications without effective treatment. Acer truncatum Bunge Seed extract (ASO) is reported to have effect on cognitive improvement, but its molecular mechanisms on HIE are unclear. In this study, ASO administration contributed to reduced neuronal cell edema and improved motor ability in HIE rats at a simulated 4500-meter altitude. Transcriptomics and WGCNA analysis showed genes associated with lipid biosynthesis, redox homeostasis, neuronal growth, and synaptic plasticity regulated in the ASO group. Targeted and untargeted-lipidomics revealed decreased free fatty acids and increased phospholipids with favorable ω-3/ω-6/ω-9 fatty acid ratios, as well as reduced oxidized glycerophospholipids (OxGPs) in the ASO group. Combining multi-omics analysis demonstrated FA to FA-CoA, phospholipids metabolism, and lipid peroxidation were regulated by ASO treatment. Our results illuminated preliminary metabolism mechanism of ASO ingesting in rats, implying ASO administration as potential intervention strategy for HIE under high-altitude.

Lipidomics reveal the cognitive improvement effects of Acer truncatum Bunge seed oil on hypoxic-ischemic encephalopathy rats.

Hypoxic-ischemic encephalopathy (HIE) is one of the leading causes of acute neonatal death and chronic neurological damage, and severe HIE can have secondary sequelae such as cognitive impairment and cerebral palsy, for which effective interventions are lacking. In this study, we found that continuous 30-day intake of Acer truncatum Bunge seed oil (ASO) reduced brain damage and improved cognitive ability in HIE rats. Using lipidomic strategies, we observed that HIE rats had decreased unsaturated fatty acids and increased lysophospholipids in the brain. However, after 30 days of ASO treatment, phospholipids, plasmalogens, and unsaturated fatty acids increased, while lysophospholipids and oxidized glycerophospholipids decreased in both serum and the brain. Enrichment analysis showed that ASO intake mainly affected sphingolipid metabolism, fat digestion and absorption, glycerolipid metabolism and glycerophospholipid metabolic pathways in serum and the brain. Cluster, correlation, and confirmatory factor analyses showed that cognitive improvement after ASO administration was attributed to increased essential phospholipids and ω3/6/9 fatty acids, coupled with decreased oxidized glycerophospholipids in HIE rats. Our findings indicate that ASO has the potential to be developed as an effective food supplement for ischemic hypoxic newborns.

Elevation of plasma soluble human leukocyte antigen-G in patients with chronic hepatitis C virus infection.

The subversion of immune responses that hepatitis C virus (HCV) uses to escape immune surveillance and to establish persistent infection has been poorly understood. The immune-suppressive molecule human leukocyte antigen-G (HLA-G) has been supposed to play important roles in viral infection. In the current study, HCV genotype was analyzed in 67 chronic HCV-infected (CHC) patients. Plasma soluble sHLA-G (including sHLA-G1 and HLA-G5), interleukin-10 (IL-10), and interferon-γ (IFN-γ) levels were determined in these CHC patients and in healthy subjects by enzyme-linked immunosorbent assay, and the sHLA-G isoforms present in plasma were determined by Western blot. Data showed that HCV 1b was the predominant genotype, with a prevalence of 64.2%. sHLA-G was dramatically increased in CHC patients (median: 85.54 U/ml, range: 19.40-204.07) over that in normal controls (median: 9.13 U/ml, range: 5.07-69.56) (p < 0.001). Western blotting revealed that plasma sHLA-G was derived from sHLA-G1 and HLA-G5. IL-10 and IFN-γ levels were also significant higher in CHC patients than in normal controls (median: 16.3 pg/ml vs 1.8 pg/ml, p < 0.001, and 1025.3 pg/ml vs 858.3 pg/ml, p = 0.03, respectively). No significant association was observed for the HCV genotype and viral RNA load with the levels of sHLA-G, IL-10, and IFN-γ in CHC patients. These results indicate that elevation of sHLA-G expression in HCV patients was independent of viral genotype and viral RNA load. Given its immunotolerant property, an increase in sHLA-G may play a role in the persistency of HCV infection.