Ning Zhu

Baicalin has protective effects against a range of cardiovascular conditions, such as myocardial ischemia-reperfusion injury, cardiac dysfunction, and apoptosis in cardiomyocytes. However, the underlying protective mechanisms in diabetic cardiomyopathy (DCM) remain unclear. The present study aimed to investigate the specific molecular mechanism activated by baicalin to ameliorate DCM. The effects of baicalin were investigated in vitro and its potential targets and pathways were identified using network pharmacology, molecular docking, echocardiography, reverse transcription PCR, ELISA, histopathology, immunofluorescence staining and western blotting. Baicalin significantly alleviated high-glucose (HG)-induced injury in H9c2 cells by inhibiting fibrotic markers, inflammatory factors and pyroptosis. Moreover, protein tyrosine phosphatase non-receptor type 22 (PTPN22) and tumor necrosis factor (TNF) were identified as crucial targets for baicalin. Molecular docking indicated that baicalin exhibited a strong binding affinity for PTPN22 and TNF. Baicalin successfully suppressed HG-induced pyroptosis, inflammation and fibrotic markers in addition to inhibiting the activation of TNF-α and PTPN22 signaling pathways. In addition, PTPN22-small interfering RNA treatment modulated pyroptosis in vitro. The present study offers insight into the key therapeutic mechanisms activated by baicalin, and its potential therapeutic targets, PTPN22 and TNF-α.

The relationship between aromatic amines (AA)s and depressive disorder remains elusive. The aim of this investigation was to examine the potential link between urinary AA levels and the likelihood of depression in American adults. Through the analysis of data from 1175 participants in the 2013–2014 NHANES, our study delved into the association between urinary AA levels and the incidence of depression. Assessment of depression severity was conducted using the PHQ-9 questionnaire, alongside measuring levels of six urinary AAs. We explored this correlation in the overall population and various subgroups by employing a multivariable logistic model, restricted cubic spline (RCS) analysis, and a sensitivity analysis model while adjusting for potential confounding variables. Participants diagnosed with depression exhibited elevated levels of 1-Aminonaphthalene, 2-Aminonaphthalene and 2,6-Dimethylaniline compared to non-depressed individuals. Specifically, the presence of 2-Aminonaphthalene was correlated with an elevated likelihood of depression in continuous and categorical models (OR: 1.013, CI: 1.004–1.023, p = 0.006; Q4 vs. Q1: OR: 1.687, CI: 1.015–2.805, p = 0.037) after fully adjusted for gender, RIP, education level, BMI, smoking, hypertension and diabetes. The likelihood of depression showed a statistically significant linear dose-response relationship with 2-Aminonaphthalene (Plinear = 0.001) after adjusting for confounding variables. Furthermore, subgroup analyses showed revealed a correlation between urinary 2-Aminonaphthalene levels and depression among female individuals and smokers, which remained consistent with sensitivity analyses. Elevated levels of certain amino acids in urine were associated with a higher likelihood of depression. Notably, 2-aminonaphthalene appeared to be a significant contributing factor, particularly among smokers.

Background: Heart failure is closely correlated with diabetic cardiomyopathy (DCM) and can lead to mortality. Celastrol has long been utilized for the treatment of immune and inflammatory disorders. However, whether celastrol would exert protective effects on DCM has not been determined. This work aimed to explore the protective actions of celastrol on DCM and unravel the underlying mechanisms involved. Methods: A DCM model was constructed in mice by intraperitoneal administration of streptozotocin. ELISA and echocardiography were performed to examine myocardial injury markers and cardiac function, respectively. Morphological changes and fibrosis were assessed using H&E staining and Masson’s staining. Inflammatory cytokines and fibrotic markers were detected by ELISA and RT-PCR. Endothelial nitric oxide synthase, apoptosis, and reactive oxygen species were detected by microscopic staining. Network pharmacology approaches, molecular docking analysis, ELISA, and Western blot were used for mechanism studies. Results: Celastrol alleviated diabetes-induced cardiac injury and remodeling. Celastrol also suppressed diabetes-induced production of inflammatory cytokines and reactive oxygen species, as well as cardiomyocyte apoptosis. The cardioprotective effects of celastrol were associated with its inhibition on the angiotensin-converting enzyme / angiotensin II / angiotensin II receptor type 1 signaling pathway. Conclusion: Celastrol exhibits significant potential as an effective cardioprotective drug for DCM treatment. The underlying mechanisms can be attributed to the blockage of celastrol on the angiotensin-converting enzyme signaling pathway.

Background: Irritable bowel syndrome (IBS) is a chronic disorder of the gut-brain axis with significant morbidity. Triptolide, an active compound extracted from Tripterygium wilfordii Hook F (TwHF), has been widely used as a major medicinal herb in the treatment of inflammatory disease. Methods: The chronic-acute combined stress (CAS) stimulation was used to establish IBS rat model. The model rats were then gavaged with triptolide. Forced swimming, marble-burying, fecal weight and abdominal withdrawal reflex (AWR) score were recorded. Pathologic changes in the ileal and colonic tissues were validated by hematoxylin and eosin staining. The inflammatory cytokines and Ornithine Decarboxylase-1 (ODC1) in the ileal and colonic tissues were performed by ELISA and WB. Results: Triptolide didn’t have antidepressant- and antianxiety- effects in rats caused by CAS, but decreased fecal weight and AWR score. In addition, Triptolide reduced the release of IL-1, IL-6, and TNF-α and the expression of ODC1 in the ileum and colon. Conclusion: The therapeutic efficacy of triptolide for IBS induced by CAS was revealed in this study, which may be related to the reduction of ODC1.

Background: Maladaptive inflammation is implicated in the development of diabetic cardiomyopathy (DCM). This study aimed to visually analyze the global scientific output over the past two decades regarding research on inflammation associated with DCM.Methods: All relevant articles and reviews were retrieved in the Web of Science (WOS) Core Collection (limited to SCIE) using “inflammation” and “diabetic cardiomyopathy” as search terms. Articles and reviews published from 1 January 2001 to 28 February 2021 were collected. Visualization analysis and statistical analysis were conducted by Microsoft 365 Excel and VOSviewer 1.6.18.Results: A total of 578 documents were finally selected for further analysis. The publications regarding inflammation and DCM increased gradually over approximately 20 years. The most prolific country was China, with 296 documents and the most citations (9,366). The most influential author groups were Lu Cai and Yihui Tan who were from the United States. The bibliometric analysis of co-occurrence keywords showed that inflammation in DCM is composed of numerous molecules (NF-κB, NLRP3 inflammasome, Nrf-2, TNF-α, protein kinase C, PPARα, TLR4, p38 mitogen-activated protein kinase, TGF-β, Sirt1, and AKT), a variety of cardiac cell types (stem cell, fibroblast, and cardiomyocyte), physiological processes (apoptosis, oxidative stress, autophagy, endoplasmic reticulum stress, hypertrophy, mitochondrion dysfunction, and proliferation), and drugs (sulforaphane, metformin, empagliflozin, and rosuvastatin).Conclusion: Our bibliometric analysis presents the characteristics and trends of inflammation in DCM and shows that research on inflammation in DCM will continue to be a hotspot.

肠易激综合征(irritable bowel syndrome, IBS)是一种常见的功能性肠病, 主要表现为反复发作的腹痛伴排便频率和(或)粪便性状改变, 腹痛常在排便后缓解, 全球发病率呈逐年上升趋势. IBS引起的肠道症状(如便秘、腹泻、腹痛、腹胀等)及其伴随的一般神经系统功能的改变会显著降低患者的生活质量和工作效率, 并造成一系列高额的医疗费用. 因此, 寻找安全、有效、经济的治疗方案成为近年的研究热点. 研究表明IBS患者和健康受试者的肠道菌群有所不同, 调节IBS患者的肠道菌群可治疗IBS. 本综述的目的是总结益生菌、益生元、合生元通过调节肠道菌群治疗IBS的应用与最新进展.

Graphical Gal-3 triggers myocardial apoptosis, oxidative stress, inflammatory cytokines release, macrophage infiltration, and fibrosis, leading to cardiac dysfunction in DCM mice.