Parkinson's disease (PD) is a serious neurodegenerative disorder wherein changes in metabolites related to lipids, glutathione, and energy metabolism occur. Currently, metabolite changes in PD have been reported, yet their role in the prognosis of disease remains poorly understood. Functional metabolites can be used to diagnose diseases, especially PD, and can exert neuroprotective effects. This study used a PD animal model and a lipopolysaccharide (LPS)—mediated inflammatory response model (using the BV-2 mouse microglial cell line) to identify functional metabolites that can identify important metabolic disorders during PD, and comprehensively evaluated their profiles using a metabolomics-based approach. Our results showed that co-treatment with myristic acid and heptadecanoic acid downregulated the expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α in BV-2 cells. Additionally, myristic acid and 10 μM heptadecanoic acid significantly inhibited the LPS-induced inflammatory response through the nuclear factor-κB pathway in BV-2 microglial cells, which provides a potential approach for PD treatment. Myristic acid and heptadecanoic acid were the active metabolites found by active metabolomics technology, but at present, there is no research report about their function for PD treatment, and our findings offer a novel research strategy for PD diagnosis and treatment.

Sepsis is one of the most important problems to be addressed in pediatrics, characterized by insidious onset, rapid progression, and high rates of severe infection and even mortality. Biomarkers with high sensitivity and robustness are urgently required for the early diagnosis of infant sepsis. Serum metabolomic approaches based on liquid chromatography-mass spectrometry were used to analyze the samples from 30 infants with sepsis at an early stage and 30 infants with noninfectious diseases. Multivariate statistical analysis was used to screen for differential metabolites and ROC curves were generated to find potential biomarkers. Six metabolites, including phosphatidic acid (PA (8:0/14:0)), phosphatidyl ethanolamine (PE (16:0/18:2(9Z,12Z))), cytidine 5'-diphosphocholine (CDP-CHO), sphingomyelin (SM (d18:0/16:1(9Z))), prolylhydroxyproline and phosphorylcholine (P-CHO), were identified between the two groups. ROC curve analysis showed that prolylhydroxyproline (AUC = 0.832) had potential diagnostic values for infant sepsis. The AUC value was 0.859 (CI: 0.764, 0.954) in the combined model. Prolylhydroxyproline were found to be correlated with CRP and PCT levels, while PE and CDP-CHO associated with PCT levels. Pathway analysis indicated that glycerophospholipid metabolism, aminoacyl-tRNA biosynthesis and necroptosis pathways played important roles in infant sepsis. Network analysis showed that the differential metabolites were linked to ERK/ MAPK, NF-κB, AMPK, mTOR, and other classical inflammatory and metabolic signaling pathways. This study identified serum metabolite profiles and three metabolites as potential biomarkers in infants with sepsis. The findings will help improve the early diagnosis of sepsis in infants.

Background: The extraction of impacted mandibular third molars might cause large bone defects in the distal area of second molars. A new strategy was innovatively employed here combining autologous bone, Bio-Oss, concentrated growth factors (CGF) gel and CGF membrane for bone repair, and the present study aimed at exploring safety as well as short- and long-term efficacy of this new protocol clinically. Materials and methods: A total of 66 participants were enrolled in this randomized single-blind clinical trial, and randomly allocated to control group (only blood clots), test A group (autogenous bone, Bio-Oss with barrier membrane) and test B group (autogenous bone, Bio-Oss, CGF gel with CGF membrane). The postoperative outcomes including PoSSe scale, periodontal probing depth (PD), degree of gingival recession and computed tomography measurements were assessed at 3rd, 6th, 12th month. A p-value < 0.05 was considered statistically significant. Results: In PoSSe scale, no significant difference was observed except a significant alleviation of early-stage pain perception in test B group (p < 0.05). Also, test B group exhibited better effect on periodontal healing and gingival recession reduction after 6 months (p < 0.05). Both two test groups showed more new bone formation than the control group (p < 0.05). It is noteworthy that the bone repair of test B group was significantly better than that of test A at 3rd and 6th month (p < 0.05), yet no difference was observed at 12th month (p > 0.05). Conclusion: Both two test groups could achieve stable long-term efficacy on bone defect repair. The use of CGF gel and CGF membrane could accelerate early-stage bone repair, alleviate short-term pain after surgery, reduce long-term probing depth and relieve economic cost for patients. This new bone repair protocol is worthy of promoting by clinicians. Trial registration: This study was registered with the identification number ChiCTR2300068466 on 20/02/2023 at Chinese Clinical Trial Registry. Also, it was ethically approved from the institutional ethics committee at the Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China (No:2023-010-01), and has been conducted in accordance to the guidelines of the declaration of Helsinki. Written informed consent was obtained from all participants in the study.

This article examines berberine’s biological effects and molecular mechanisms with an inflammatory response model induced by lipopolysaccharide (LPS) in human gingival fibroblasts (HGFs) using metabolomics. The viability of HGFs was determined using the cell counting kit-8 (CCK8). ELISA was used to measure inflammatory cytokines, including interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor- α (TNF-α). An investigation of western blots was conducted to investigate the related proteins of apoptosis. Low concentrations of berberine (0.1, 0.5, and 1 μmol L⁻¹) did not affect HGF growth, whereas high concentrations of berberine (5–25 μmol L⁻¹) significantly activated cell proliferation. Berberine suppressed the elevated secretion of IL-6, IL-1β, and TNF-α induced by LPS in HGF. Western blot analysis showed that 10 μmol L⁻¹ of berberine significantly inhibited LPS-induced apoptosis signaling pathway activation. Our results suggested that berberine could inhibit LPS-induced apoptosis and the production of proinflammatory mediators in HGFs cells. Berberine may be a potential therapeutic drug for the management of periodontitis.