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Aim of this research was to examine the impact of paeoniflorin (Pae) in suppressing the occurrence of ferroptosis in individuals with Alzheimer's disease (AD). The study utilized APP/PS1 mice with AD as the experimental subjects. Following the administration of Pae, the cognitive behaviors of mice were evaluated and the key indexes of ferroptosis were measured, as well as levels of oxidative stress (OS). For in‐vitro experiments, Erastin was adopted for inducing the ferroptosis of PC12 cells, and the level of cell ferroptosis was detected after Pae treatment. Pae improved the cognitive ability of AD mice, reduced the level of ferroptosis, decreased the iron ion and MAD levels in brain tissues, and increased SOD expression. In PC12 cells, Pae suppressed the Erastin‐induced ferroptosis, mitigated oxidative damage, and reduced the level of ROS. Based on the findings from our research, it was observed that Pae exhibited a specific binding affinity to P53, leading to the suppression of ferroptosis. This mechanism ultimately resulted in the improvement of nerve injury in mice with AD. [ABSTRACT FROM AUTHOR]

This work aimed to investigate the role and mechanism of NADPH oxidase 4 (NOX4) in the polarization of microglial cells. Microglial cells were transfected with the NOX4 overexpression plasmid (pGL3‐NOX4), and later treated with lipopolysaccharide (LPS) and interferon‐γ (IFN‐γ) to induce its M1 polarization. Later, the F4/80 + CD86 + cell proportion was detected by flow cytometry (FCM), the inflammatory factor expression levels were analyzed through enzyme‐linked immunosorbent assay (ELISA), while ionized calcium binding adapter molecule 1 (IBA‐1) and PKM2 expression were measured by immunofluorescence (IF) staining. In addition, dichlorodihydrofluorescein diacetate probe was utilized to detect the reactive oxygen species (ROS) levels, glucose uptake, and glycolysis, as well as lactic acid level. The expression of glycolytic enzymes PKM2, HK2, and citrate (Si)‐synthas (CS) was detected by Western‐blot (WB) assay. Moreover, the polarization level of microglial cells was detected after ROS expression was suppressed by the ROS inhibitor N‐acetylcysteine (NAC). In mouse experiments, LPS was applied in inducing central neuroinflammation in NOX4 knockdown mouse model (KO) and wild‐type mice (WT). Thereafter, the inflammatory factor levels and lactic acid level in mouse tissues were detected; IBA‐1 and CD86 expression in mice was measured by IF staining; and the expression of glycolytic enzymes PKM2, HK2, and CS in the central nervous system (CNS) was also detected. After NOX4 overexpression in microglial cells, the M1 polarization level was upregulated, the F4/80 + CD86 + cell proportion increased, and inflammatory factors were upregulated. At the same time, the expression of glycolytic enzymes PKM2, HK2, and CS was upregulated. NAC pretreatment suppressed the effects of NOX4, reduced the F4/80 + CD86 + cell proportion, and suppressed the expression of PKM2, HK2, and CS. In the mouse model, the expression levels of CD86 in KO group decreased, and the inflammatory factors were also downregulated. NOX4 promotes glycolysis of microglial cells via ROS, thus accelerating M1 polarization and inflammatory factor expression. In this regard, NOX4 is promising as a new target for the treatment of neuroinflammation. Highlight: 1.NOX4 can promote microglial cells M1 polarization.2.NOX4 promotes glycolysis of microglial cells via reactive oxygen species, thus accelerating M1 polarization and inflammatory factor expression.3.NOX4 is promising as a new target for neurological treatment. [ABSTRACT FROM AUTHOR]

M1 microglia predominated in AD mice, which promoted the inflammatory cytokine expressions significantly. The microglia can clear A through phagocytosis and release pro-inflammatory cytokines and cytotoxic substances.4 In AD, microglia polarize to pro-inflammatory M1 phenotype upon stimulation. Nevertheless, RBAP can significantly reduce the proportion of M1 cells and inhibit the inflammatory cytokine expressions in M1 cells. [Extracted from the article]

Introduction: The study was designed to assess the expression of long non-coding RNA HOTAIR (lncRNA HOTAIR) in tissues and peripheral blood of patients with advanced hepatocellular carcinoma (HCC). In addition, we also investigated the prognostic correlation between the expression level of lncRNA HOTAIR in tumour tissues and peripheral blood of patients with advanced HCC and sunitinib monotherapy.Material and Methods: A total of 60 patients with advanced HCC who received sunitinib monotherapy and another 60 healthy individuals who were examined at the physical examination centre during the same period were included in the study. Real-time quantitative PCR (RT-QPCR) was used to determine the relative expression of lncRNA HOTAIR in tumour tissue, adjacent tissue, and peripheral blood of HCC patients as well as peripheral blood of healthy controls. Moreover, the clinicopathological information, overall survival (OS), and progression-free survival (PFS) were collected, followed by correlation analysis with lncRNA HOTAIR expression.Results: The expression of lncRNA HOTAIR was significantly higher in tumour tissues compared to that in adjacent tissues (t = 9.03, p < 0.001). The expression of lncRNA HOTAIR in peripheral blood of HCC patients was higher than that in healthy controls (t = 8.04, p < 0.001). There was a correlation between the expression of lncRNA HOTAIR in tumour tissue and peripheral blood in HCC patients (r = 0.638, p < 0.001). Patients with low lncRNA HOTAIR expression in tumour tissues harboured significantly longer OS (13.4 vs. 9.5, p < 0.001) and PFS (8.4 vs. 6.2, p < 0.001) compared to those with high expression. Consistently, patients with low lncRNA HOTAIR expression in peripheral blood had significantly prolonged OS (12.8 vs. 9.1, p < 0.001) and PFS (8.9 vs. 6.4, p < 0.001) compared to those with high expression. Patients with low expression both in tumour tissue and peripheral blood had prolonged OS (14.3 vs. 8.8, p < 0.001) and PFS (10.6 vs. 6.0, p < 0.001) compared to the rest of the patients. Cox regression analysis indicated that the expression level of lncRNA HOTAIR in tumour tissue and peripheral blood was an independent predictive factor of OS and PFS in patients with advanced HCC treated by sunitinib.Conclusions: The expression of lncRNA HOTAIR was up-regulated in tumour tissue and peripheral blood in patients with advanced HCC. In addition, the expression level of lncRNA HOTAIR was one of the indicators predicting the effectiveness of sunitinib therapy. [ABSTRACT FROM AUTHOR]

This work aimed to investigate the effect of aurantiamide (Aur) in promoting the M2 polarization of microglial cells to improve the cognitive ability of mice with Alzheimer's disease (AD). The M2 polarization of BV2 cells was induced by interleukin-4 (IL-4) treatment.Aur promoted the M2 polarization of BV2 cells, and up-regulated the expression of CD206 and SOCS3. In the meantime, it increased TGF-β1, Arg-1 and IL-10 levels, and promoted the polarization of JAK1-STAT6. Treatment with STAT6 inhibitor antagonized the effect of Aur. Besides, the cognitive ability of AD mice was improved after Aur treatment, meanwhile, the expression of CD206 was up-regulated, while that of IBA-1 was down-regulated. Aur promotes the M2 polarization of microglial cells to improve the cognitive ability of AD mice, and such effect is related to the STAT6 signal., (© 2022 John Wiley & Sons Ltd.)

Introduction: The study was designed to assess the expression of long non-coding RNA HOTAIR (lncRNA HOTAIR) in tissues and peripheral blood of patients with advanced hepatocellular carcinoma (HCC). In addition, we also investigated the prognostic correlation between the expression level of lncRNA HOTAIR in tumour tissues and peripheral blood of patients with advanced HCC and sunitinib monotherapy., Material and Methods: A total of 60 patients with advanced HCC who received sunitinib monotherapy and another 60 healthy individuals who were examined at the physical examination centre during the same period were included in the study. Real-time quantitative PCR (RT-QPCR) was used to determine the relative expression of lncRNA HOTAIR in tumour tissue, adjacent tissue, and peripheral blood of HCC patients as well as peripheral blood of healthy controls. Moreover, the clinicopathological information, overall survival (OS), and progression-free survival (PFS) were collected, followed by correlation analysis with lncRNA HOTAIR expression., Results: The expression of lncRNA HOTAIR was significantly higher in tumour tissues compared to that in adjacent tissues ( t = 9.03, p < 0.001). The expression of lncRNA HOTAIR in peripheral blood of HCC patients was higher than that in healthy controls ( t = 8.04, p < 0.001). There was a correlation between the expression of lncRNA HOTAIR in tumour tissue and peripheral blood in HCC patients ( r = 0.638, p < 0.001). Patients with low lncRNA HOTAIR expression in tumour tissues harboured significantly longer OS (13.4 vs. 9.5, p < 0.001) and PFS (8.4 vs. 6.2, p < 0.001) compared to those with high expression. Consistently, patients with low lncRNA HOTAIR expression in peripheral blood had significantly prolonged OS (12.8 vs. 9.1, p < 0.001) and PFS (8.9 vs. 6.4, p < 0.001) compared to those with high expression. Patients with low expression both in tumour tissue and peripheral blood had prolonged OS (14.3 vs. 8.8, p < 0.001) and PFS (10.6 vs. 6.0, p < 0.001) compared to the rest of the patients. Cox regression analysis indicated that the expression level of lncRNA HOTAIR in tumour tissue and peripheral blood was an independent predictive factor of OS and PFS in patients with advanced HCC treated by sunitinib., Conclusions: The expression of lncRNA HOTAIR was up-regulated in tumour tissue and peripheral blood in patients with advanced HCC. In addition, the expression level of lncRNA HOTAIR was one of the indicators predicting the effectiveness of sunitinib therapy., Competing Interests: The authors declare no conflict of interest., (Copyright: © 2021 Termedia & Banach.)

Objective: To study the protective effects of polysaccharides on myocardial ischemia reperfusion injury in rats after preconditioning., Methods: The myocardial ischemia reperfusion model was established by reversible left anterior descending coronary artery ligation: 0. 5 h was myocardial ischemia and 2 h was re perfused. A total of 50 healthy SD rats were randomly divided into 5 groups: sham operation group, model group, polysaccharide high dose group, polysaccharide middle dose group and polysaccharide low dose group, 10 rats in each group. The polysaccharide group was given 100, 50, 10 mg/kg of camphora polysaccharides at 30 min before operation, while the model group and the sham operation group were treated with equal dose of saline. The expression of malondialdehyde( MDA), catalase( CAT), superoxide dismutase( SOD), creatine kinase( CK) and creatine kinase isoenzyme( CK-MB) in serum of rats and tumor necrosis factor alpha( TNF-α), interleukin-1β( IL-1β) 、interleukin-6( IL-6) in myocardial tissue were detected by Elisa method. The expression of Bcl-2, Bax and Caspase-3 in myocardium was detected by Western-Blot. The infarct size and myocardial tissue HE staining were measured., Results: Compared with the model group, the infarct size of the rats pretreated with polysaccharides decreased significantly, The levels of MDA, CK, CK-MB in serum and TNF-α, IL-1, IL-6 in myocardium were significantly decreased. The expression of SOD and CAT in serum increased significantly. The expression of Bax and caspase-3 was decreased and the expression of Bcl-2 was elevated in myocardium. HE staining showed that the injury degree of myocardial tissue in pretreated rats treated with polysaccharide was significantly lower than that in model group., Conclusion: Polysaccharide can reduce the apoptosis of myocardial cells by resisting oxidative stress and inflammatory damage, play a protective role in rats of Myocardial ischemia reperfusion injury.

Resting-state functional magnetic resonance imaging (R-fMRI) signals are spatiotemporally organized. R-fMRI studies in patients with classic trigeminal neuralgia (CTN) have suggested alterations in functional connectivity. However, far less attention has been given to investigations of the local oscillations and their frequency-specific changes in these patients. The objective of this study was to address this issue in patients with CTN. R-fMRI data from 17 patients with CTN and 19 age- and gender-matched healthy controls (HCs) were analyzed using amplitude of low-frequency fluctuation (ALFF). The ALFF was computed across different frequencies (slow-4: 0.027-0.073 Hz; slow-5: 0.01-0.027 Hz; and typical band: 0.01-0.08 Hz) in patients with CTN compared to HCs. In the typical band, patients with CTN showed increases of ALFF in bilateral temporal, occipital, and left middle frontal regions and in the left middle cingulate gyrus, as well as decreases of ALFF in the right inferior temporal region and in regions (medial prefrontal regions) of default mode network. These significant group differences were identified in different sub-bands, with greater brainstem findings in higher frequencies (slow-4) and extensive default mode network and right postparietal results in lower frequencies (slow-5). Furthermore, significant relationships were found between subjective pain ratings and both amplitudes of higher frequency (slow-4) blood oxygen level-dependent (BOLD) signals in pain localization brain regions and lower frequencies (slow-5) in pain signaling/modulating brain regions in the patients, and decreased ALFF within the prefrontal regions was significantly correlated with pain duration in the patients. This result supports our hypothesis that trigeminal pain has a characteristic spatiotemporal distribution of low-frequency BOLD signals. These findings might contribute to a better understanding of the impact of CTN on the brain's intrinsic architecture. Future studies should take the frequencies into account when measuring brain resting BOLD signals of patients with CTN., Competing Interests: Disclosure The authors report no conflicts of interest in this work.