Neuroinflammation is considered a risk factor for impairments in neuronal function and cognition that arise with trauma, infection, and/or disease. IL-17A has been determined to be involved in neurodegenerative diseases such as multiple sclerosis. Recently, IL-17A has been shown to be upregulated in lipopolysaccharide(LPS)-induced systemic inflammation. This study aims to explore the role of IL-17A in LPS-induced neuroinflammation and cognitive impairment. Male Sprague–Dawley (SD) rats were injected intraperitoneally with LPS (500 μg/kg), and IL-17A expression in serum and in the hippocampus was examined 6, 12, 24, and 48 h later. Then, we investigated whether IL-17A-neutralizing antibodies (IL-17A Abs, 1 mg/kg) prevented neuroinflammation and memory dysfunction in aged rats that received LPS (500 μg/kg) injection. In addition, the effect of IL-17A on microglial activation in vitro was determined using ELISA and immunofluorescence. LPS injection increased the expression of IL-17A in serum and in the hippocampus. IL-17A Abs improved LPS-induced memory impairment. In addition, IL-17A Abs prevented the LPS-induced expression of TNF-α, IL-6 and inflammatory proteins, and of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) as well as the activation of microglia in the brain. IL-17A Abs also inhibited the expression of amyloid precursor protein (APP) and BACE1 and increased the expression of the synaptic marker PSD95 in the aged rats treated with LPS. In an in vitro study, we found that recombinant IL-17A could simulate microglial activation and increase production of pro-inflammatory cytokines. Taken together, our results suggest that IL-17A was involved in LPS-induced neuroinflammation and cognitive impairment in aged rats via microglial activation. Anti-IL-17A may represent a new therapeutic strategy for the treatment of endotoxemia-induced neuroinflammation and cognitive dysfunction.

Objectives: This systematic review and meta-analysis was conducted to identify the potential risk factors for postoperative delirium in geriatric patients with hip fracture.Methods: PubMed, EMBASE, and Cochrane Library were searched from inception until December 31st, 2021. A combined searching strategy of subject words and free words was adopted. Studies involving risk factors for postoperative delirium in elderly patients undergoing hip fracture surgeries were reviewed. Qualities of included studies were assessed using the Newcastle–Ottawa Scale. Data were pooled and a meta-analysis was performed using Review Manager 5.3.Results: A total of 37 studies were included. The following risk factors were significant: advanced age (per year increase) (OR: 1.05, 95% CI 1.04–1.07), age>80 years (OR: 2.26, 95% CI 1.47–3.47), male (OR: 1.53, 95% CI 1.37–1.70), preoperative cognitive impairment (OR:3.20, 95% CI 2.12–4.83), preoperative dementia (OR: 2.74, 95% CI 2.18–3.45), preoperative delirium (OR: 9.23, 95% CI 8.26–10.32), diabetes (OR: 1.18, 95% CI 1.05–1.33), preoperative functional dependence (OR: 1.31, 95% CI 1.11–1.56), ASA level (per level increase) (OR: 1.63, 95% CI 1.04–2.57), ASA level≥3(OR: 1.76, 95% CI 1.39–2.24), low albumin (OR: 3.30, 95% CI 1.44–7.55), medical comorbidities (OR: 1.15, 95% CI 1.06–1.25), Parkinson's disease (OR: 4.17, 95% CI 1.68–10.31) and surgery delay>48 h (OR: 1.90, 95% CI 1.36–2.65).Conclusions: Clinicians should be alert to patients with those risk factors. To identify the risk factors more precisely, more research studies with larger sample size and better design should be conducted.

Postoperative cognitive dysfunction (POCD), as one of the common postoperative complications, mainly occurs after surgery and anesthesia, especially in the elderly. It refers to cognitive function changes such as decreased learning and memory ability and inability to concentrate. In severe cases, there could be personality changes and a decline in social behavior. At present, a great deal of research had been carried out on POCD, but its specific mechanism remains unclear. The release of peripheral inflammation‐related factors, the degradation and destruction of the blood‐brain barrier, the occurrence of central inflammation, and the neuronal apoptosis and synaptic loss could be promoted by neuroinflammation indicating that inflammatory mechanisms may play key roles in the occurrence of POCD.

Background: Metabolic-associated fatty liver disease (MAFLD) has risen as one of the leading etiologies for hepatocellular carcinoma (HCC). Oncogenes have been suggested to be responsible for the high risk of MAFLD-related HCC. We analyzed the impact of the proto-oncogene c-MYC in the development of human and murine MAFLD and MAFLD-associated HCC. Methods: alb-myc^tg mice were studied at baseline conditions and after administration of Western diet (WD) in comparison to WT littermates. c-MYC expression was analyzed in biopsies of patients with MAFLD and MAFLD-associated HCC by immunohistochemistry. Results: Mild obesity, spontaneous hyperlipidaemia, glucose intolerance and insulin resistance were characteristic of 36-week-old alb-myc^tg mice. Middle-aged alb-myc^tg exhibited liver steatosis and increased triglyceride content. Liver injury and inflammation were associated with elevated ALT, an upregulation of ER-stress response and increased ROS production, collagen deposition and compensatory proliferation. At 52 weeks, 20% of transgenic mice developed HCC. WD feeding exacerbated metabolic abnormalities, steatohepatitis, fibrogenesis and tumor prevalence. Therapeutic use of metformin partly attenuated the spontaneous MAFLD phenotype of alb-myc^tg mice. Importantly, upregulation and nuclear localization of c-MYC were characteristic of patients with MAFLD and MAFLD-related HCC. Conclusions: A novel function of c-MYC in MAFLD progression was identified opening new avenues for preventative strategies.