Studies have found that salidroside, isolated from Rhodiola rosea L, has various pharmacological activities, but there have been no studies on the effects of salidroside on brain hippocampal senescence. The purpose of this study was to investigate the mechanistic role of salidroside in hippocampal neuron senescence and injury. In this study, long‐term cultured primary rat hippocampal neurons and naturally aged C57 mice were treated with salidroside. The results showed that salidroside increased the viability and MAP2 expression, reduced β‐galactosidase (β‐gal) levels of rat primary hippocampal neurons. Salidroside also improved cognition dysfunction in ageing mice and alleviated neuronal degeneration in the ageing mice CA1 region. Moreover, salidroside decreased the levels of oxidative stress and p21, p16 protein expressions of hippocampal neurons and ageing mice. Salidroside promoted telomerase reverse transcriptase (TERT) protein expression via the phosphatidylinositol‐3‐kinase (PI3K)/protein kinase B (Akt) pathway. In conclusion, our findings suggest that salidroside has the potential to be used as a therapeutic strategy for anti‐ageing and ageing‐related disease treatment.

Ischemic stroke is a common cerebrovascular disease and recovering blood flow as early as possible is essential to reduce ischemic damage and maintain neuronal viability, but the reperfusion process usually causes additional damage to the brain tissue in the ischemic area, namely ischemia reperfusion injury. The accumulated studies have revealed that transplantation of exogenous neural stem cells (NSCs) is an ideal choice for the treatment of ischemia reperfusion injury. At present, the source and efficacy of exogenous NSCs after transplantation is still one of the key issues that need to be resolved. In this study, human umbilical cord mesenchymal stem cells (hUC-MSCs) were obtained and induced into NSCs byadding growth factor and neuregulin1β (NRG1β) was introduced during the differentiation process of NSCs. Then, the rat middle cerebral artery occlusion/reperfusion (MCAO/R) models were established, and the therapeutic effects were evaluated among groups treated by NRG1β, NSCs and NSCs pretreated with 10 nM NRG1β (NSCs-10 nM NRG1β) achieved through intra-arterial injection. Our data show that the NSCs-10 nM NRG1β group significantly improves neurobehavioral function and infarct volume after MCAO/R, as well as cerebral cortical neuron injury, ferroptosis-related indexes and mitochondrial injury. Additionally, NSCs-10 nM NRG1β intervention may function through regulating the p53/GPX4/SLC7A11 pathway, and reducing the level of ferroptosis in cells, further enhance the neuroprotective effect on injured cells.

Background: Previous studies have investigated circulating fetuin-B and its association with type 2 diabetes mellitus (T2DM). However, the variation and regulatory factors of serum fetuin-B levels in individuals with metabolic syndrome (MetS) have not been explained. This study evaluated circulating fetuin-B concentrations in newly diagnosed individuals with MetS and analyzed the impacts of blood glucose, insulin, and glucagon-like peptide-1 receptor agonists (GLP-1RA) treatment on circulating fetuin-B in vivo.Methods: A total of 377 women (192 MetS and 185 healthy subjects) were recruited for cross-sectional study. The euglycemic-hyperinsulinemic clamp (EHC) and oral glucose tolerance test (OGTT) were implemented in healthy women and those with MetS. Serum fetuin-B were examined by an ELISA kit. For the GLP-1RA intervention experiment, twenty-four women with MetS were treated with Liraglutide for 6 months. Results: Serum fetuin-B levels were markedly higher in women with MetS as compared to healthy women. Circulating fetuin-B reflected a positive correlation with body mass index, waist hip ratio (WHR), the percentage of fat in vivo (FAT%), triglyceride, fasting blood glucose, 2-hour blood glucose after glucose overload, glycosylated hemoglobin, fasting plasma insulin, 2-hour plasma insulin after glucose overload, homeostasis model assessment of insulin resistance (HOMA-IR), visceral adiposity index (VAI), and lipid accumulation product (LAP). Multivariate linear regression analyses demonstrated that triglyceride and WHR were independently related factors of serum fetuin-B. Serum fetuin-B levels were related to MetS by binary logistic regression analysis. In fact, serum fetuin-B was markedly elevated in healthy women after glucose loading and in MetS women during the EHC. After six months of GLP-1RA intervention, serum fetuin-B levels in MetS subjects decreased following improvement of metabolism and insulin sensitivity. Conclusions: Serum fetuin-B levels were associated with MetS and its components and regulated by glucose and insulin. GLP-1RA treatment can reduce serum fetuin-B levels in women with MetS. Clinical Trial Registration Number: ChiCTR-OCS-13003185. Registered 02/01 2016, http://www.chictr.org.cn/showproj.aspx?proj=6374

Background: Fibroblast growth factor 19 (FGF19) secrets from intestinal epithelial cells and proved to be associated with functioning ileum in Crohn’s disease and alcoholic steatohepatitis. In the present study, we aimed to explore the potential value of FGF19 as a biomarker for assessment of gastrointestinal (GI) dysfunction in pediatric patients with sepsis.Methods: We performed a prospective study to enroll pediatric patients with sepsis admitted to the pediatric intensive care unit (PICU) at Shanghai Children’s Hospital from January 2018 to December 2018. Serum FGF19 levels at PICU admission were determined, and the clinical and laboratory parameters were collected.Results: Significantly decreased serum FGF19 levels were found in patients with sepsis-associated GI dysfunction. Lower serum FGF19 levels than 60 μg/mL on PICU admission is predictive for GI dysfunction. Correlation analyses revealed significant correlations of serum FGF19 with hemoglobin, and low FGF19 serum concentration less than 52 μg/mL on PICU admission is related to GI dysfunction-associated liver injury. Conclusion: Serum FGF19 is a novel predictor for GI dysfunction or GI-liver dysfunction in pediatric patients with sepsis.

Introduction: Vascular dementia (VaD), one of the brain injuries, is difficult to be cured, so it is important to take active neuroprotective treatment after its occurrence. Many studies have shown that apoptosis serves an important role in VaD occurrence; therefore, inhibition of apoptosis may contribute to the recovery of neurological function after VaD occurrence. Cerebroprotein hydrolysate-I (CH-I), a neuropeptide preparation which consists of several amino acids and small molecular peptides as the main active constituent, is extracted using a method similar to cerebrolysin (CBL) which has neuroprotective and neurotrophic effects. Methods: In the present study, a VaD model which was constructed using bilateral common carotid artery occlusion (BCCAO) in Kunming mice was applied to examine the neuroprotective effects of CH-I. Results:The results show that CH-I treatment could attenuate the decrease of learning and memory ability, cell apoptosis in the hippocampal CA1 region and inhibit the activation of caspase-3 and caspase-9 in VaD mice. Furthermore, CH-I treatment could also upregulate Bcl-2 protein levels and activate PI3K and Akt. Discussion: We speculate that CH-I may induce a neuroprotective effect activating PI3K/ Akt signaling pathway in VaD mice.