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Background: Systemic inflammation has been implicated in the pathogenesis of moyamoya disease (MMD). Sortilin is a critical regulator of proinflammatory cytokine secretion in several cell types. The present study investigated the association between circulating sortilin and proinflammatory cytokine levels and the occurrence of MMD., Methods: Forty-two MMD cases and 76 age- and sex-matched controls were enrolled in this study between January 2018 and June 2019 at the Affiliated Hospital of Jining Medical University. The demographic and clinical characteristics were evaluated, and the circulating serum and cerebrospinal fluid (CSF) levels of sortilin, sortilin-related receptor with A-type repeats (SorLA), and proinflammatory cytokines including C-reactive protein (CRP), interleukin (IL)-6, interferon (IFN)-γ were measured by enzyme-linked immunosorbent assay. Linear regression and correlation analyses were used to estimate the associations between sortilin, SorLA, and proinflammatory cytokine levels., Results: MMD patients had higher serum levels of sortilin (P = 0.012), CRP (P = 0.013), IL-6 (P = 0.004), and IFN-γ (P = 0.033) than healthy controls. In MMD patients, serum sortilin was positively correlated with serum proinflammatory cytokines (CRP: r = 0.459, P = 0.0022; IL-6: r = 0.445, P = 0.0032; and IFN-γ: r = 0.448, P = 0.0029) and CSF sortilin (r = 0.440, P = 0.0035); the latter was positively correlated with CSF levels of CRP (r = 0.542, P = 0.0002), IL-6 (r = 0.440, P = 0.0036), and IFN-γ (r = 0.443, P = 0.0033)., Conclusions: Elevated sortilin level is associated MMD onset and may be a clinically useful biomarker along with proinflammatory cytokine levels.

Background: Rheumatoid synovial inflammation occurs at the synovial joint, which is activated by the articular system and mediated by the immune cells. In the case of untreated rheumatoid arthritis, the inflammation may affect the extra-articular system including cardiovascular, hepatic, respiratory, circulatory, and neuromuscular systems, which may ultimately interfere with the quality of life of patients with rheumatoid arthritis. This, in turn, reduces the life expectancy of the patient. Materials and Methods: The effectiveness of asiaticoside was evaluated by the Freund's complete adjuvant (FCA)-induced rheumatoid arthritis model using experimental Wistar rats. According to our results, asiaticoside exhibited potent anti-arthritic activity in contrast to the control animals in the FCA-induced rheumatoid arthritic model. Results: The parameters of arthritis such as reduced body weight, increased paw volume and pro-inflammatory cytokines, and cartilage destruction were significantly (P < 0.05) affected by the administration of asiaticoside. It significantly (P < 0.01) increased the body weight, decreased the paw volume and pro-inflammatory cytokines, restored the blood components, increased the levels of antioxidant enzymes, and protected the cartilage. Conclusion: Asiaticoside exhibited potential anti-arthritic activity against FCA-induced rheumatoid arthritis in experimental rats. [ABSTRACT FROM AUTHOR]

Purpose: An increasing body of evidence reveals that inflammation is involved in the pathological mechanisms of depression. Our previous basic research confirmed that Dl-3-n-butylphthalide (NBP) possess anti-inflammatory properties. However, studies investigating metabolite biomarkers for the involvement of NBP in hippocampus tissue in the lipopolysaccharide (LPS)-induced rat model of depression are currently limited. Thus, the aim of this study was to identify metabolite biomarkers in the hippocampus for the impact of NBP in this model of depression. Material and methods: Male Sprague–Dawley rats were randomly allocated to one of the following three groups (n=6): Control, LPS-induced rat model of depression (LPS), and NBP involvement in the LPS-induced rat model of depression (LPS+NBP). Ultra-high-performance liquid chromatography-mass spectroscopy was used to determine the hippocampal metabolites. Multivariate statistical analysis was performed to identify differentially expressed hippocampal metabolites in the three groups. Results: Most of the identified differentially expressed metabolites were related to amino acid, lipid, energy, and oxidative stress metabolism. Additionally, metabolites were eventually connected to different pathways and metabolic networks, which may partly account for the pathophysiological process of depression. Conclusion: The present findings provide insight into the anti-inflammatory effects of NBP, and further elucidate the pathophysiological mechanisms underlying inflammation-induced depression. [ABSTRACT FROM AUTHOR]

• Our study is the first study to report changes in hippocampus lipids following NBP treatment in the LPS-induced rat model of depression. • Our lipidomic analysis provided important lipid biomarker candidates for depression and the NBP involvement in depression. • Our study demonstrated that most of the differentially expressed lipid metabolites were involved in four metabolic pathways. Elevated inflammation is commonly observed in depression, but whether this association is causal is not determined. Our previous basic research indicated that Dl-3 -n- butylphthalide (NBP) possessed an anti-inflammatory effect. Additional recent evidence consistently suggests that depression is associated with lipid metabolism. Therefore, our study performed an untargeted lipidomics approach of ultra-performance liquid chromatography coupled with mass spectrometry (UPLC-MS) to reveal the potential discriminating lipid profile of the hippocampus for NBP involvement in lipopolysaccharide (LPS)-induced depression. Male Sprague-Dawley(SD) rats were randomly allocated to one of three groups (n = 6): control, LPS-induced model of depression (LPS), or NBP involvement in the LPS-induced model of depression (LPS + NBP). Statistical analysis was used to identify differential hippocampus lipids in the LPS, NBP + LPS, and control groups. Our study demonstrated that most of the differentially expressed lipid metabolites were involved in glycerophospholipid metabolism, sphingolipid metabolism, glycerolipid metabolism, and glycosylphosphatidylinositol(GPI)-anchor biosynthesis, which may partially account for the pathophysiological process of depression. However, more pre-clinical and clinical evidence is warranted to determine the extent and consistency of the role of NBP and further elucidate the pathophysiological mechanisms underlying inflammation-induced depression. [ABSTRACT FROM AUTHOR]