Gateshartvig9758

In molecular docking analyses, NBP bound to NLRP3, interleukin-1β, caspase-1, Foxp3, and Ki-67. These results demonstrate that NBP reduces neuroinflammation in brain tissues and promotes nerve and blood vessel regeneration, thus protecting neuromorphology and function.Parkinson's disease (PD) is a common age-related neurodegenerative disease that affects the structural architecture of the cerebral cortex. Cortical thickness (CTh) via surface-based morphometry (SBM) analysis is a popular measure to assess brain structural alterations in the gray matter in PD. However, the results of CTh analysis in PD lack consistency and have not been systematically reviewed. We conducted a comprehensive coordinate-based meta-analysis (CBMA) of 38 CTh studies (57 comparison datasets) in 1,843 patients with PD using the latest seed-based d mapping software. Compared with 1,172 healthy controls, no significantly consistent CTh alterations were found in patients with PD, suggesting CTh as an unreliable neuroimaging marker for PD. The lack of consistent CTh alterations in PD could be ascribed to the heterogeneity in clinical populations, variations in imaging methods, and underpowered small sample sizes. These results highlight the need to control for potential confounding factors to produce robust and reproducible CTh results in PD.Microglia are the resident immune cells in the central nervous system and play an essential role in brain homeostasis and neuroprotection in brain diseases. Exosomes are crucial in intercellular communication by transporting bioactive miRNAs. Thus, this study aimed to investigate the function of microglial exosome in the presence of ischemic injury and related mechanism. Oxygen-glucose deprivation (OGD)-treated neurons and transient middle cerebral artery occlusion (TMCAO)-treated mice were applied in this study. Western blotting, RT-PCR, RNA-seq, luciferase reporter assay, transmission electron microscope, nanoparticle tracking analysis, immunohistochemistry, TUNEL and LDH assays, and behavioral assay were applied in mechanistic and functional studies. The results demonstrated that exosomes derived from microglia in M2 phenotype (BV2-Exo) were internalized by neurons and attenuated neuronal apoptosis in response to ischemic injury in vitro and in vivo. BV2-Exo also decreased infarct volume and behavioral deficits in ischemic mice. Exosomal miRNA-137 was upregulated in BV2-Exo and participated in the partial neuroprotective effect of BV2-Exo. Furthermore, Notch1 was a directly targeting gene of exosomal miRNA-137. In conclusion, these results suggest that BV2-Exo alleviates ischemia-reperfusion brain injury through transporting exosomal miRNA-137. This study provides novel insight into microglial exosomes-based therapies for the treatment of ischemic brain injury.Long non-coding RNAs (lncRNA) play a vital role in colorectal cancer (CRC) progression. To investigate the role of long intergenic non-coding RNA LINC00485 in CRC, we performed in vitro functional experiments. LoVo tumor-bearing and liver metastasis mice were used as in vivo models. We found that LINC00485 expression was significantly lower in CRC tissues and cancer cells than in paired normal samples and human normal colonic epithelial cells. Lower expression of LINC00485 predicted poor prognosis in CRC patients. LINC00485 knockdown promoted the proliferation, migration, and invasion of FHC cells, while LINC00485 overexpression weakened these abilities of LoVo cells. MicroRNA miR-581 was the downstream target of LINC00485, which was downregulated in CRC samples and cancer cells compared to normal tissues and normal colonic epithelial cells. MiR-581 overexpression induced proliferation, migration, and invasion of FHC cells, while miR-581 antagomir treatment produced opposite results. MiR-581 directly targeted the 3'UTR of EDEM1 and inhibited its expression and induction of epithelial-mesenchymal transition of CRC. In mouse models, LINC00485 knockdown or down-regulation of miR-581 significantly repressed CRC cell growth and prevented CRC liver metastasis. Overall, LINC00485 suppressed CRC tumorigenesis and progression by targeting the miR-581/EDEM1 axis. LINC00485 may be a potential therapeutic target for CRC.Bony injuries lead to compromised skeletal functional ability which further increase in aging population due to decreased bone mineral density. see more Therefore, we aimed to investigate the therapeutic potential of platelet-derived biomaterials (PDB) against bone injury. Specifically, we assessed the impact of PDB on osteo-inductive characteristics and migration of mouse embryonic fibroblasts (MEFs). Osteogenic lineage, matrix mineralization and cell migration were determined by gene markers (RUNX2, OPN and OCN), alizarin Red S staining, and migration markers (FAK, pFAK and Src) and EMT markers, respectively. The therapeutic impact of TGF-β1, a key component of PDB, was confirmed by employing inhibitor of TGF-β receptor I (Ti). Molecular imaging-based in vivo cellular migration in mice was determined by establishing bone injury at right femurs. Results showed that PDB markedly increased expression of osteogenic markers, matrix mineralization, migration and EMT markers, revealing higher osteogenic and migratory potential of PDB-treated MEFs. In vivo cell migration was manifested by expression of migratory factors, SDF-1 and CXCR4. Compared to control, PDB-treated mice exhibited higher bone density and volume. Ti treatment inhibited both migration and osteogenic potential of MEFs, affirming impact of TGF-β1. Collectively, our study clearly indicated PDB-rescued bone injury through enhancing migratory potential of MEFs and osteogenesis.Altered trunk movements during gait in persons with lower-limb amputation are often associated with an increased risk for secondary health conditions; however, the postural control strategies underlying such alterations remain unclear. In this secondary analysis, the authors employed nonlinear measures of triplanar trunk accelerations via short-term Lyapunov exponents to investigate trunk local stability as well as spatiotemporal gait parameters to describe gait mechanics. The authors also evaluated the influence of a concurrent task on trunk local stability and gait mechanics to explore if competition for neuromuscular processing resources can assist in identifying unique strategies to control kinematic variability. Sixteen males with amputation-8 transtibial and 8 transfemoral-and 8 uninjured males (controls) walked on a treadmill at their self-selected speed (mean = 1.2 m/s ±10%) in 5 experimental conditions (8 min each) 4 while performing a concurrent task (2 walking and 2 seated) and 1 with no concurrent task. Individuals with amputation demonstrated significantly smaller Lyapunov exponents than controls in all 3 planes of motion, regardless of concurrent task or level of amputation (P less then .0001). Individuals with transfemoral amputation walked with wider strides compared with individuals with transtibial amputation and controls (P less then .0001). Individuals with amputation demonstrated more trunk kinematic variability in the presence of wider strides compared with individuals without amputation, and it appears that performing a concurrent cognitive task while walking did not change trunk or gait mechanics.

Hypertension is the highest risk factor for disease globally. When prescription of drug therapy is recommended, patients might decline treatment due to hypertension asymptomatic nature, sometimes turning to alternative therapies. One popular therapy is berberine, a plant alkaloid that has been used in eastern medicine for millennia to treat several ailments, including cardiovascular diseases and their risk factors.

Through a transparent and pragmatic approach towards searching, synthesising, assessing, and reporting the available clinical evidence, the present review aimed to investigate berberine effect on blood pressure and cardiovascular disease risk. It also intended to provide guidance for clinician when advising their patients, and to highlight gaps in the research along offering suggestions to fill them.

The review was conducted following the protocol PRISMA-P, and reported according to the related PRISMA statement. The PICO framework was used to define the scope of the review, and to arrive at as cardiovascular events, mortality, and adverse outcomes.

The evidence around berberine effect on blood pressure is limited, of low quality, and ultimately inconclusive. Clinicians should be aware that the evidence from randomised trials is not sufficient to establish berberine effectiveness and safety in the treatment of hypertension, and they should balance these findings with the long history of berberine use in the Eastern world. Researchers should aim at improving quality of studies, by raising the standard of designing and reporting them, e.g., by following the CONSORT guidelines, and strive to measure meaningful clinical endpoints, such as cardiovascular events, mortality, and adverse outcomes.

Over the years, roles of microRNAs (miRNAs) in development of human diseases has been broadly investigated, while the role of dexmedetomidine (DEX) regulating miR-381-5p in myocardial ischemia-reperfusion injury (MIRI) remains largely unknown. Thus, we aimed to identify the effect of DEX on MIRI via mediating miR-381-5p.

The MIRI mice models were established by the ligation of the left anterior descending (LAD) artery and treated with miR-381-5p agomir, silenced chitinase-3-like 1 protein (CHI3L1) and DEX. The cardiac function, serum inflammatory factors, pathological changes and cardiomyocyte apoptosis of the mice' myocardial tissues were measured. The targeting relationship between miR-381-5p and CHI3L1 was predicted.

MiR-381-5p expression was decreased while CHI3L1 expression was increased in myocardial tissues of MIRI mice. DEX preconditioning could improve cardiac function and attenuate the pathological changes, cardiomyocyte apoptosis in myocardial tissues and inflammatory response in serum of MIRI mice. MiR-381-5p agomir improved the protective impact of DEX on myocardial injury in MIRI mice. Moreover, there existed a target relation between miR-381-5p and CHI3L1.

Our study demonstrated that upregulated miR-381-5p strengthens the effect of DEX preconditioning to protect against MIRI in mouse models by inhibiting CHI3L1.

Our study demonstrated that upregulated miR-381-5p strengthens the effect of DEX preconditioning to protect against MIRI in mouse models by inhibiting CHI3L1.

Chronic obstructive pulmonary disease (COPD) is a disease associated with accelerated aging that threatens the lives of people worldwide and imposes heavy social and economic burdens. Cellular senescence is commonly observed in COPD and contributes to aging-related diseases.

To identify the possible molecular pathways modulating cellular senescence in COPD.

MiR-494-3p expression levels in COPD tissues, small airway epithelial cells (SAECs) and BEAS-2B cells were detected by qRT-PCR. After transfection with miR-494-3p mimic or inhibitor in COPD SAECs, miR-494-3p modulation of senescence markers and senescence-associated secretory phenotype (SASP) proteins was detected. A luciferase assay was employed to verify the direct binding of SIRT3 and miR-494-3p. VX745 and c-myc siRNA were used to investigate the regulation of p38MAPK and c-myc by miR-494-3p.

As a result of oxidative stress, MiR-494-3p was increased via the p38MAPK-c-myc signaling pathway in the lung tissues and cells of patients with COPD, and the increase in miR-494-3p was accompanied by increases in senescence markers (p27, p21 and p16) and SASP proteins (IL-1β, TNF-α, MMP2 and MMP9).