A serious neurosurgical emergency, subarachnoid hemorrhage (SAH) is characterized by vascular and neuropathy, as well as complex pathological mechanisms like vascular lesions, inflammatory responses, and nerve cell damage. The inflammatory response is an essential aspect of SAH's pathophysiology, causing the release of a number of inflammatory mediators and oxidative stress products like TNF-α, MCP-1, MMPs, and so on, which either directly or indirectly contribute to the development of SAH.It has recently been discovered that some antibodies against inflammatory mediators, antioxidant stress, botanicals, and traditional Chinese medicine decrease the inflammatory response of SAH. Additionally, certain biomarkers linked to inflammation may serve as a foundation for clinical diagnosis.Although these mechanisms are still not completely understood, we can explore potential therapeutic targets by studying the role of inflammatory responses and bioactive molecules in the formation of SAH.

Objective: To explore the bidirectional association between dyslipidemia and depression, and the potential predictive role of lipid level changes for depression onset. Methods: A systematic search of the Cochrane Library, Web of Science, Embase, and PubMed databases was conducted to identify cohort studies on blood lipids and 5-hydroxytryptamine (5-HT) parameters related to depression, from database inception to May 2024. Data were analyzed using Stata 14.0 software. Results: Seven studies were included in the analysis. Serum high-density lipoprotein (HDL) and triglyceride levels are significantly associated with an increased risk of depression (OR = 1.28, 95% CI: 1.07 - 1.53; OR = 1.41, 95% CI: 1.20 - 1.66, P < 0.05). However, depressive symptoms do significantly affect serum HDL, LDL, triglyceride, or total cholesterol levels (ORs = 0.88, 1.05, 1.05, 1.11; 95% CIs: 0.58 - 1.35, 0.88 - 1.24, 0.91 - 1.21, 0.9 - 1.32, P > 0.05). Conclusion: Based on the present findings, changes in serum HDL and triglyceride levels are significantly linked to depression incidence. Monitoring these two lipid parameters may aid in early identification of at-risk individuals and enhance the prognosis and quality of life for depressed patients through timely interventions. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/ , identifier CRD42024542833.

Objective: Cognitive impairment (CI) is highly prevalent in subarachnoid hemorrhage (SAH) patients. The phosphatidylinositol 3-kinase (PI3K)/AKT pathway plays a critical role in neuronal survival in a variety of central nervous system injuries. This study aimed to determine whether electroacupuncture (EA) at Yintang and LI20 ameliorates SAH-CI in a rat model and to examine whether it modulates the PI3K/AKT pathway by administering a PI3K inhibitor (LY294002) versus dimethyl sulfoxide (DMSO) vehicle. Methods: Notably, 129 male Sprague–Dawley rats were divided into Blank, Sham, SAH and SAH + EA groups (Experiment 1, n = 54) and SAH, SAH + EA, SAH + LY294002, SAH + EA + LY294002 and SAH + EA + DMSO groups (Experiment 2, n = 75). Garcia scoring was used to evaluate neurological function. The moisture content of the rat brain was determined by dry‒wet method. The Morris water maze was used to assess learning and memory function. Pathological changes in neurons in the hippocampus were observed via hematoxylin–eosin (H&E) staining. The number of surviving neurons and the percentage of apoptotic cells in the hippocampus were detected via Nissl and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining. The expression of PI3K/AKT pathway-related proteins was detected via Western blotting. Results: The results indicated that EA intervention after SAH reduced brain water content, enhanced Garcia scores, improved neurological function and behavioral markers of CI, and increased the number of surviving neurons in the hippocampus. Moreover, EA significantly increased the expression of AKT, phosphorylated (p)-AKT, PI3K, p-PI3K, glycogen synthase kinase (GSK)-3β, p-GSK-3β and B cell lymphoma (Bcl)-2 proteins, and decreased the expression of Bcl-2-associated X (Bax) and caspase-3. In addition, the effects of EA were abolished by LY294002. Conclusion: EA appeared to improve CI in a rat model of SAH through the activation of the PI3K/AKT pathway.