Sepsis-induced acute kidney injury (AKI) continues to be associated with poor outcomes in critical care patients. Previous research has revealed that tetrahydrocurcumin (THC) exerts renoprotective effects in multiple nephritic disorders by modulating inflammation and oxidative stress. However, the effects of THC on sepsis-induced AKI and the underlying mechanisms remain unclear. In this study, a mouse model of sepsis-induced AKI, generated by cecal ligation and puncture operation, was used to investigate the protective effects of THC and the role of SIRT1. Histological manifestation and TUNEL analysis were observed to determine the severity of kidney damage. Levels of BUN, SCr, KIM-1, and UAlb/Cr were calculated to assess the renal function. Expressions of IL-1β, IL-6, and TNF-α were measured to evaluate the inflammatory response. MDA content, SOD, GSH, CAT, and GPx activities and DHE staining were analyzed to estimate the degree of oxidative stress. Protein expressions of SIRT1, Ac-p65, and Ac-foxo1 were detected to explore the underlying mechanisms. We observed that THC not only increased the survival rate, improved the kidney function and ameliorated the renal histological damage of septic mice, but also inhibited inflammatory response, prohibited oxidative stress, and prevented cell apoptosis in renal tissues in septic mice. Mechanistically, THC remarkably increased the expression of SIRT1, accompanied by decreased expressions of downstream molecules Ac-p65 and Ac-foxo1. Meanwhile, the beneficial effects of THC were clearly abolished by the SIRT1-specific inhibitor EX527. These results delineate that THC prevents sepsis-induced AKI by suppressing inflammation and oxidative stress through activating the SIRT1 signaling. Abbreviation: Ac-p65: acetylated p65; Ac-foxo 1: acetylated forkhead box O1; AKI: acute kidney injury; BUN: blood urea nitrogen; CAT: catalase; DHE: dihydroethidium; GPx: glutathione peroxidase; GSH: reduced glutathione; IL-1β: Interleukin-1 beta; IL-6: Interleukin-6; KIM-1: kidney injury molecule 1; MDA: malondialdehyde; SCr: serum creatinine; SIRT1: silent information regulator 1; SOD: superoxide dismutase; THC: tetrahydrocurcumin; TNF-α: tumor necrosis factor-alpha; TUNEL: TdT-mediated dUTP Nick-End Labeling; UAlb/Cr: urine micro albumin/creatinine.

Background: Community-acquired pneumonia (CAP) leads to high morbidity and mortality among the elderly, with 3 million deaths annually worldwide. Multiple comorbidities significantly increase the risk. This study aims to identify independent risk factors for mortality in elderly patients with CAP to optimize individualized treatment strategies.Methods: This single-center retrospective study was conducted at First Affiliated Hospital of Xi’an Medical University. Clinical data from elderly patients diagnosed with CAP between December 2018 and December 2023 were retrospectively collected. Logistic regression analysis was used to determine risk factors for in-hospital mortality. A nomogram was constructed based on the final model for risk assessment.Results: A total of 613 eligible patients were included, with 68.2% being male, and a median age of 78 (IQR 70–86) years. The prevalence of hypertension, coronary heart disease (CHD), stroke, diabetes, malignancy, and chronic obstructive pulmonary disease (COPD) was 55.5, 39.8, 29.5, 27, 16.6, and 7%, respectively. The in-hospital mortality rate was 48%. Compared to survivors, non-survivors were older, had a higher proportion of males, faster heart rates, and higher rates of comorbidities. Multivariate logistic regression analysis identified age (OR 1.05, 95% CI [1.02–1.07], P < 0.01), BMI (OR 0.92, 95% CI [0.86–0.98], P < 0.01), stroke (OR 2.21, 95% [1.43–3.42], P < 0.01), ARDS (OR 4.0, 95% CI [2.17–7.37], P < 0.01), AKI (OR 2.98, 95% CI [1.77–5.01], P < 0.01), malignancy (OR 2.11, 95% CI [1.22–3.65], P < 0.01), elevated WBC (OR 1.20, 95% [1.14–1.27], P < 0.01), PLT (OR 0.995, 95% CI [0.993–0.998], P < 0.01), and albumin (OR 0.93, 95% CI [0.90–0.97], P < 0.01) as independent risk factors for in-hospital mortality. The area under the curve (AUC) of the multivariable model was 0.85 (95% CI [0.81–0.87], P < 0.01).Conclusion: Elderly CAP patients have a high prevalence of comorbidities and a high in-hospital mortality rate. Advanced age, low BMI, stroke, ARDS, AKI, malignancy, elevated WBC, decreased PLT, and low albumin were independent risk factors for in-hospital mortality.

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Objects: Taurine exhibits protective effects in the context of cardiovascular pathophysiology. A range of evidence suggests that hypertension activates inflammatory responses and oxidative stress in the paraventricular nucleus (PVN), elevating the arterial tone and sympathetic activity, while it induces gut–brain axis dysfunction in the context of hypertension. However, the mechanism underlying taurine’s anti-hypertensive effects via the gut–brain axis remains unclear. Method: Male spontaneously hypertensive rats (SHRs) were administered 3% taurine in their drinking water for eight weeks, with their arterial pressure measured weekly. Molecular techniques were employed to investigate taurine’s effects on the hypertensive gut and PVN. Additionally, 16S rRNA gene sequencing was used to analyze the gut microbiota composition, and untargeted metabolomics was applied to assess the fecal metabolites following taurine supplementation. Results: Taurine supplementation not only reduced the blood pressure, sympathetic activity, and inflammatory and oxidative stress in the PVN but also improved the cardiac pathology and microbiota composition while alleviating gut inflammation in hypertensive rats. The untargeted metabolite analysis indicated that the primary effect of the taurine intervention in SHRs was exerted on tryptophan metabolism. The levels of serum metabolites such as kynurenine, L-tryptophan, serotonin (5-HT), and 5-hydroxyindole-3-acetic acid (5-HIAA) were altered in hypertensive rats following taurine treatment. Conclusions: Taurine supplementation restored the microbiota balance, strengthened the mucosal barrier, reduced intestinal inflammation, and stimulated tryptophan metabolism. The metabolites derived from the gut microbiota likely crossed the brain barrier and reached the paraventricular nucleus, thereby reducing the inflammatory responses and oxidative stress in the PVN via gut–brain communication, leading to decreased sympathetic nerve activity and blood pressure in the studied hypertensive rats.

Background: Heart failure (HF) is a primary cause of death in patients on maintenance hemodialysis (MHD), yet the role of microbial dysbiosis is poorly defined. This study characterized the salivary and gut microbiomes of MHD patients with heart failure with preserved ejection fraction (HFpEF), those without HF (NHF), and healthy controls (CON). Methods: In this cross-sectional study (n=88), we compared the salivary and fecal microbiomes of HFpEF (n=30), NHF (n=30), and CON (n=28) groups using 16S rRNA gene sequencing. Microbial community structure and composition were analyzed. Results: Alpha diversity and Beta diversity analysis revealed a distinct salivary microbial structure, which effectively distinguished the MHD group from the Con group (P < 0.05). Conversely, the overall gut community structure showed no significant separation. At the genus level, both MHD groups showed depletion of salivary Veillonella and gut Faecalibacterium compared to controls. Notably, LEfSe analysis highlighted salivary Anaerocolumna as a promising candidate feature associated with the HFpEF group. Conclusion: Our analyses suggest that HFpEF in MHD patients may be associated with structural alterations in the oral microbiome, which appear more pronounced than those in the gut. Specific oral microbial signatures, particularly the enrichment of Anaerocolumna, showed associations with the HFpEF cohort in our study. This preliminary evidence positions the oral microbiome as an area worthy of further investigation for its potential role in this high-risk population.