Effectiveness of patient decision aids in patients with advanced kidney disease: a meta-analysis based on randomized controlled trials.

PURPOSE: To systematically evaluate the decision effectiveness of patient decision aids (PtDAs) on the decision-making effect of patients with advanced chronic kidney disease. METHOD: Two authors independently searched ten electronic databases [Web of science, PubMed, the Cochrane Library, Embase, CINAHL, EBSCO, CBM, CNKI, WanFang DATA and Vip database], to include randomized controlled trials of interventions through PtDAs in patients with advanced chronic kidney disease published from the inception of the database until April 2024. Two authors conducted a comprehensive quality evaluation (Cochrane 5.1.0) before independently extracting and analyzing the data with RevMan 5.2. RESULTS: The study included 11 randomized controlled trials with a total of 1613 patients. According to the results, PtDAs can improve the decision knowledge [SMD = 0.53, 95% CI (0.26, 0.80), P = 0.0002] and decision preparation [SMD = 2.34, 95% CI (2.04, 2.65), P < 0.00001] of patients with advanced chronic kidney disease. Additionally, there was a substantial decrease in the levels of decision regret [SMD = - 1.33, 95% CI (- 2.11, - 0.55), P < 0.05] and decision conflict [SMD = - 0.88, 95% CI (- 1.47, - 0.28), P = 0.004]. CONCLUSION: The current available evidence indicates that PtDAs can significantly enhance the decision knowledge and decision preparation of patients with advanced chronic kidney disease. Additionally, PtDAs can reduce the levels of decision regret and decision conflict. TRIAL REGISTRY: CRD42023433798.

The Tao Hong Si Wu Decoction ameliorates diabetes-associated cognitive dysfunction by inhibiting the formation of amyloid plaques.

OBJECTIVES: The herbs in Tao Hong Si Wu Decoction (THSWD) are beneficial in the treatment of cognitive impairment. However, the underlying mechanisms of THSWD in treating diabetes-associated cognitive dysfunction (DACD) are not entirely explored. This study is aimed to investigate the therapeutic effects of THSWD in DACD model rats and the underlying mechanism. METHODS: Ultra-high-phase liquid chromatography was employed to identify the main compounds contained in the THSWD extract. DACD rat model was induced by feeding with a high-sugar and high-fat diet and injecting streptozotocin (35 mg/kg). DACD rats were gavaged with THSWD for 1 week. The learning and memory abilities of the rats were measured by using the Morris water maze. Western blotting was used to detect the changes in DACD rat targets. Statistical methods were used to evaluate the correlation between proteins. RESULTS: The results show that THSWD effectively reduced the escape latency, hippocampal neuron damage, glycosylated hemoglobin, type A1C, and blood lipid levels in DACD rats. Furthermore, DACD rats showed significantly increased amyloid precursor protein, ß-secretase, Aß1-40 , Aß1-42 , Tau phosphorylation, and advanced glycation end products (AGEs) expression. However, THSWD treatment can reverse this phenomenon. CONCLUSIONS: THSWD can improve the learning and memory abilities of DACD rats by inhibiting the expression of AEGs-AGE receptors pathway, which provides an experimental basis for the clinical application of THSWD. In addition, the experiment combines pharmacological and statistical methods, which offers a new perspective for the study of Chinese herbal medicine.

Structural characterization and antioxidant activity of processed polysaccharides PCP-F1 from Polygonatum cyrtonema Hua.

Introduction: Polygonatum cyrtonema Hua. (PC) is a traditional Chinese herb with a history of use in both food and medicine. For clinical use, processed PC pieces are most commonly used, while present research has focused on crude PC polysaccharides (PCPs). Methods: In this study, a new polysaccharide, PCP-F1, with a molecular weight of 37.46 kDa, was separated from four-time processed PCPs by column chromatography and evaluated by antioxidant activity. It was composed of glucose, mannose, galactose, rhamnose, and galacturonic acid with a molar ratio of 3.5: 2.5: 1.3: 1.8: 0.8. Results and Discussion: The methylation analysis and two-dimensional NMR measurement revealed that the configuration of PCP-F1 contained nine residues in the primary structural unit by the chain of →3)-α-D-Glcp, →2)-α-D-Glcp (6→, →1)-ꞵ-D-Glcp (2→, →2)-α-D-GalAp (3,4→, →1) -ꞵ-D-Manp (3→, →2)-α-D-Glcp (3→, branched for →3)-α-D-Glcp, →2)-ꞵ-D-Galp (4→, →1)-ꞵ-D-Glcp (2→, →2,4)-α-D-Manp (6→, →3)-α-L-Rhap (4→. Radical scavenging assays indicated that PCP-F1 could scavenge radicals with a high scavenging rate, suggesting PCP-F1 possesses good antioxidant activity. The study confirms the importance of processed PC and offers the potential for exploiting it as a functional food.

Bakuchiol ameliorates cerebral ischemia-reperfusion injury by modulating NLRP3 inflammasome and Nrf2 signaling.

Cerebral ischemia/reperfusion (I/R) injury is a common cerebrovascular disease with high mortality. Bakuchiol (BAK), extracted from the seeds of psoralea corylifolia, exhibits anti-inflammatory effects on lung, kidney and heart injuries. However, the effect of BAK on brain I/R injury remains elusive. In our study, a cerebral I/R model in mice was established by 1-h middle cerebral artery occlusion and 24-h reperfusion (1-h MCAO/24-h R). Prior to it, mice were gavaged with BAK (2.5 or 5 mg/kg) per day for 5 days. BAK pre-treatment improved neurological deficit, and reduced infarct volume, cerebral edema and neuronal injury in MCAO/R-injured mice. BAK decreased the number of Iba1-immunoreactive cells in the brain, indicating a reduction of microglial activation. BAK also reduced the expressions of NLRP3, ASC, cleaved-caspase-1, IL-1ß and IL-18. BAK triggered Nrf2 nuclear accumulation and elevated HO-1 level. Further, the role of BAK was explored in BV-2 microglia with 3-h oxygen-glucose deprivation/24-h reperfusion (3-h OGD/24-h R). It was found that the functions of BAK in vitro were consistent with those in vivo, as manifested by reduced NLRP3 inflammasome and activated Nrf2 signaling. In addition, BV-2 cells were treated with Brusatol, an Nrf2 inhibitor. Results showed that Brusatol partially reversed the protective effect of BAK on OGD/R-injured BV-2 cells, further confirming that BAK might exhibit its anti-inflammatory property via activating Nrf2 signaling. In short, BAK is more meaningful in improving cerebral ischemic injury through suppressing NLRP3-mediated inflammatory response and activating the Nrf2 signaling pathway.