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Thyroid cancer (TC) is the most common endocrine malignancy, with a rapidly increasing global incidence. Scutellariae Barbatae Herba (SBH) exhibits significant antitumor activity; however, its mechanism against TC remains unclear. This study aims to explore the immunotherapeutic mechanism of SBH in treating TC through network pharmacology, bioinformatics analysis, and experimental validation. In the TCMSP database, the active components and potential targets of SBH were screened to construct a drug-component-target-disease network. TC targets were then filtered, and common targets were selected to build a protein-protein interaction network. GO and KEGG enrichment analyses were performed. The expression, prognosis, and immunotherapeutic roles of core genes were validated using TCGA databases. Molecular docking demonstrated the binding interactions between core components and targets. Finally, in vitro experiments were conducted to validate the results of the network pharmacology analysis. 14 active components and 29 potential targets of SBH in treating TC were identified from the TCMSP database. PPI network analysis highlighted SPP1 as a key target. GO enrichment analysis involved 722 biological processes, 24 cellular components, and 73 molecular functions. KEGG enrichment analysis suggested that the anticancer effect of SBH might be mediated through signaling pathways such as AGE-RAGE and PI3K-Akt. TCGA data indicated that SPP1 is highly expressed in TC and is associated with diagnosis, pathological stage, N stage, and gender of TC patients. Additionally, SPP1 expression correlated with the infiltration of 24 types of immune cells, with the highest correlation observed with macrophages. Molecular docking demonstrated that SPP1 has high binding stability with quercetin, Rhamnazin, and Salvigenin, with binding energies of -8.117, -7.494, and − 7.202 kJ∙mol − 1, respectively. Experimental validation showed that quercetin inhibited the growth of TC cells in a dose-dependent manner. Protein results indicated that quercetin downregulated SPP1 mRNA and protein expression. This study combines database predictions with experimental validation to reveal the potential mechanisms of SBH against TC, providing effective strategies for the immunotherapy of TC.

Background Although the etiology of PD remains unclear, increasing evidence has shown that oxidative stress plays an important role in its pathogenesis and that of other neurodegenerative disorders. NOX2, a cytochrome subunit of NOX, transports electrons across the plasma membrane to generate ROS, leading to physiological and pathological processes. Heme oxygenase-1 (HO-1) can be rapidly induced by oxidative stress and other noxious stimuli in the brain or other tissues. Astaxanthin (ATX), a carotenoid with antioxidant properties, is 100–1000 times more effective than vitamin E. The present study investigated the neuroprotective effects of ATX on MPP + -induced oxidative stress in PC12 cells. Results MPP + significantly decreased MTT levels in a concentration-dependent manner. Hemin, SnPPIX and ATX didn’t exhibit any cytotoxic effects on PC12 cells. Pretreatment with ATX (5, 10, 20 μM), caused intracellular ROS production in the MPP + group to decrease by 13.06%, 22.13%, and 27.86%, respectively. MPP + increased NOX2, NRF2 and HO-1 protein expression compared with control (p < 0.05). Co-treatment with hemin or ATX suppressed NOX2 expression (p < 0.01), and greatly increased NRF2 and HO-1 expression (p < 0.01). MPP + treatment up-regulated both NOX2 (p < 0.01) and HO-1 (p < 0.01) mRNA levels. Co-treatment with hemin or ATX significantly increased HO-1 mRNA levels (p < 0.01), and decreased NOX2 mRNA levels (p < 0.01). MPP + increased NOX2 and HO-1 expression with considerable fluorescence extending out from the perinuclear region toward the periphery; this was attenuated by DPI. Co-treatment with hemin or ATX significantly up-regulated HO-1 expression and decreased NOX2 expression with considerable fluorescence intensity (stronger than the control and MPP + groups). Conclusions ATX suppresses MPP + -induced oxidative stress in PC12 cells via the HO-1/NOX2 axis. ATX should be strongly considered as a potential neuroprotectant and adjuvant therapy for patients with Parkinson’s disease.

Periodontitis has emerged as one of the most critical oral diseases, and research on this condition holds great importance for the advancement of stomatology. As the most authoritative national scientific research funding institution in China, the National Natural Science Foundation of China (NSFC) has played a pivotal role in driving the progress of periodontal science by supporting research on periodontitis. This article provides a comprehensive review of the research and development progress related to periodontitis in China from 2014 to 2023, highlighting the significant contributions of the NSFC to this field. We have summarized the detailed funding information from the NSFC, including the number of applicant codes, funded programs and the distribution of funded scholars. These data illustrate the efforts of the NSFC in cultivating young scientists and building research groups to address key challenges in national scientific research. This study offers an overview of the current hot topics, recent breakthroughs and future research prospects related to periodontitis in China.

Objective: To investigate astaxanthin (ATX) neuroprotection, and its mechanism, on a 1-methyl-4-phenyl-pyridine ion (MPP+)-induced cell model of Parkinson’s disease. Methods: Mature, differentiated PC12 cells treated with MPP+ were used as an in vitro cell model. The MTT assay was used to investigate cell viability after ATX treatment, and western blot analysis was used to observe Sp1 (activated transcription factor 1) and NR1 (NMDA receptor subunit 1) protein expression, real-time PCR was used to monitor Sp1 and NR1 mRNA, and cell immunofluorescence was used to determine the location of Sp1 and NR1 protein and the nuclear translocation of Sp1. Results: PC12 cell viability was significantly reduced by MPP+ treatment. The expression of Sp1 and NR1 mRNA and protein were increased compared with the control (p < 0.01). Following co-treatment with ATX and MPP+, cell viability was significantly increased, and Sp1 and NR1 mRNA and protein were decreased, compared with the MPP+ groups (p < 0.01). In addition, mithracycin A protected PC12 cells from oxidative stress caused by MPP+ by specifically inhibiting the expression of Sp1. Moreover, cell immunofluorescence revealed that ATX could suppress Sp1 nuclear transfer. Conclusion: ATX inhibited oxidative stress induced by MPP+ in PC12 cells, via the SP1/NR1 signaling pathway.

Alzheimer’s disease (AD) is the most common dementia and the trigger of its pathological cascade is widely believed to be the overproduction and accumulation of β-amyloid protein (Aβ) in the affected brain. However, effective AD remedies are still anxiously awaited. Recent evidence suggests that curcumin may be a potential agent for AD treatment. In this study, we used 5×FAD transgenic mice as an AD model to investigate the effects of curcumin on AD. Our results showed that curcumin administration (150 or 300 mg/kg/day, intragastrically, for 60 days) dramatically reduced Aβ production by downregulating BACE1 expression, preventing synaptic degradation, and improving spatial learning and memory impairment of 5×FAD mice. These findings suggest that curcumin is a potential candidate for AD treatment.

Alzheimer's disease (AD) is the most common dementia and the trigger of its pathological cascade is widely believed to be the overproduction and accumulation of [beta]-amyloid protein (A[beta]) in the affected brain. However, effective AD remedies are still anxiously awaited. Recent evidence suggests that curcumin may be a potential agent for AD treatment. In this study, we used 5×FAD transgenic mice as an AD model to investigate the effects of curcumin on AD. Our results showed that curcumin administration (150 or 300 mg/kg/day, intragastrically, for 60 days) dramatically reduced A[beta] production by downregulating BACE1 expression, preventing synaptic degradation, and improving spatial learning and memory impairment of 5×FAD mice. These findings suggest that curcumin is a potential candidate for AD treatment.

Alzheimer's disease (AD) is the most common dementia and the trigger of its pathological cascade is widely believed to be the overproduction and accumulation of beta -amyloid protein (A beta ) in the affected brain. However, effective AD remedies are still anxiously awaited. Recent evidence suggests that curcumin may be a potential agent for AD treatment. In this study, we used 5FAD transgenic mice as an AD model to investigate the effects of curcumin on AD. Our results showed that curcumin administration (150 or 300 mg/kg/day, intragastrically, for 60 days) dramatically reduced A beta production by downregulating BACE1 expression, preventing synaptic degradation, and improving spatial learning and memory impairment of 5FAD mice. These findings suggest that curcumin is a potential candidate for AD treatment.

Background: Although the etiology of PD remains unclear, increasing evidence has shown that oxidative stress plays an important role in its pathogenesis and that of other neurodegenerative disorders. NOX2, a cytochrome subunit of NOX, transports electrons across the plasma membrane to generate ROS, leading to physiological and pathological processes. Heme oxygenase-1 (HO-1) can be rapidly induced by oxidative stress and other noxious stimuli in the brain or other tissues. Astaxanthin (ATX), a carotenoid with antioxidant properties, is 100-1000 times more effective than vitamin E. The present study investigated the neuroprotective effects of ATX on MPP super(+)-induced oxidative stress in PC12 cells. Results: MPP super(+) significantly decreased MTT levels in a concentration-dependent manner. Hemin, SnPPIX and ATX didn't exhibit any cytotoxic effects on PC12 cells. Pretreatment with ATX (5, 10, 20 [mu]M), caused intracellular ROS production in the MPP super(+) group to decrease by 13.06%, 22.13%, and 27.86%, respectively. MPP super(+) increased NOX2, NRF2 and HO-1 protein expression compared with control (p < 0.05). Co-treatment with hemin or ATX suppressed NOX2 expression (p < 0.01), and greatly increased NRF2 and HO-1 expression (p < 0.01). MPP super(+) treatment up-regulated both NOX2 (p < 0.01) and HO-1 (p < 0.01) mRNA levels. Co-treatment with hemin or ATX significantly increased HO-1 mRNA levels (p < 0.01), and decreased NOX2 mRNA levels (p < 0.01). MPP super(+) increased NOX2 and HO-1 expression with considerable fluorescence extending out from the perinuclear region toward the periphery; this was attenuated by DPI. Co-treatment with hemin or ATX significantly up-regulated HO-1 expression and decreased NOX2 expression with considerable fluorescence intensity (stronger than the control and MPP super(+) groups). Conclusions: ATX suppresses MPP super(+)-induced oxidative stress in PC12 cells via the HO-1/NOX2 axis. ATX should be strongly considered as a potential neuroprotectant and adjuvant therapy for patients with Parkinson's disease.

The formations of the blue straggler stars and the FK Com-type stars are unsolved problems in stellar astrophysics. One of the possibilities for their formations is from the coalescence of W UMa-type overcontact binary systems. Therefore, deep (f > 50%), low-mass ratio (q < 0.25) overcontact binary stars are a very important source to understand the phenomena of Blue Straggler/FK Com-type stars. Recently, 12 W UMa-type binary stars, FG Hya, GR Vir, IK Per, TV Mus, CU Tau, V857 Her, V410 Aur, XY Boo, SX CrV, QX And, GSC 619-232, and AH Cnc, were investigated photometrically. Apart from TV Mus, XY boo, and GSC 619-232, new observations of the other 9 binaries were obtained. Complete light curves of the 10 systems, FG Hya, GR Vir, IK Per, TV Mus, CU Tau, V857 Her, GSC 619-232, V410 Aur, XY Boo, and AH Cnc, were analyzed with the 2003 version of the W-D code. It is shown that all of those systems are deep (f > 50%), low-mass ratio (q < 0.25) overcontact binary stars. We found that the system GSC 619-232 has the highest degree of overcontact (f = 93.4%). The derived photometric mass ratio of V857 Her, q = 0.0653, indicates that it is the lowest-mass ratio system among W UMa-type binaries. Of the 12 sample stars, long-term period changes of 11 systems were found. About 58% (seven) of the sample binaries show cyclic period oscillation. No cyclic period changes were discovered for the other 5 systems, which may be caused by the short observational time interval or by insufficient observations. Therefore, we think that all W UMa-type binary stars may contain cyclic period variations. By considering the long-term period changes (both increase and decrease) of those binary stars, we proposed two evolutionary scenarios evolving from deep, low-mass ratio overcontact binaries into Blue Straggler/FK Com-type stars.

We focus on the synchronization of a wide class of four-dimensional (4-D) chaotic systems. Firstly, based on the stability theory in fractional-order calculus and sliding mode control, a new method is derived to make the synchronization of a wide class of fractional-order chaotic systems. Furthermore, the method guarantees the synchronization between an integer-order system and a fraction-order system and the synchronization between two fractional-order chaotic systems with different orders. Finally, three examples are presented to illustrate the effectiveness of the proposed scheme and simulation results are given to demonstrate the effectiveness of the proposed method.