Preventive Effect of Royal Jelly and 10-HDA on Skin Damage in Diabetic Mice through Regulating Keratinocyte Wnt/ß-Catenin and Pyroptosis Pathway.

The objective of this study is to elucidate how Royal jelly (RJ) and 10-hydroxy-2-decanoic acid (10-HDA) prevents diabetic skin dysfunction by modulating the pyroptosis pathway. Type 2 diabetes models are induced by fat diet consumption and low dose of streptozotocin (STZ) in C57BL/6J mice and treated with RJ (100 mg kg-1 day-1) and 10-HDA, the major lipid component of royal jelly (100 mg kg-1 day-1) for 28 weeks. The results show that serum concentrations of glucose and triglyceride are significantly lower in the RJ group or 10-HDA than diabetes mellitus (DM) group. Compared to the control group, pyroptosis proteins, GSDMD, ASC, Caspase-1, and IL-1ß are increased in the skin of the diabetic model, accompanied by the activation of the Wnt/ß-catenin signal pathway. Further evaluations by RJ exhibit superior improvement of skin damage, repress activation of the Wnt/ß-catenin pathway, and attenuate keratinocyte pyroptosis, but 10-HDA cannot completely suppress the activation of Wnt/ß-catenin pathway and pyroptosis, which shows a relatively weak protective effect on skin damage which shows that RJ is a better effect on skin injury after DM.

Disulfidptosis, A Novel Cell Death Pathway: Molecular Landscape and Therapeutic Implications.

Programmed cell death is pivotal for several physiological processes, including immune defense. Further, it has been implicated in the pathogenesis of developmental disorders and the onset of numerous diseases. Multiple modes of programmed cell death, including apoptosis, pyroptosis, necroptosis, and ferroptosis, have been identified, each with their own unique characteristics and biological implications. In February 2023, Liu Xiaoguang and his team discovered "disulfidptosis," a novel pathway of programmed cell death. Their findings demonstrated that disulfidptosis is triggered in glucose-starved cells exhibiting high expression of a protein called SLC7A11. Furthermore, disulfidptosis is marked by a drastic imbalance in the NADPH/NADP+ ratio and the abnormal accumulation of disulfides like cystine. These changes ultimately lead to the destabilization of the F-actin network, causing cell death. Given that high SLC7A11 expression is a key feature of certain cancers, these findings indicate that disulfidptosis could serve as the basis of innovative anti-cancer therapies. Hence, this review delves into the discovery of disulfidptosis, its underlying molecular mechanisms and metabolic regulation, and its prospective applications in disease treatment.

The role of snapin in regulation of brain homeostasis.

Brain homeostasis refers to the normal working state of the brain in a certain period, which is important for overall health and normal life activities. Currently, there is a lack of effective treatment methods for the adverse consequences caused by brain homeostasis imbalance. Snapin is a protein that assists in the formation of neuronal synapses and plays a crucial role in the normal growth and development of synapses. Recently, many researchers have reported the association between snapin and neurologic and psychiatric disorders, demonstrating that snapin can improve brain homeostasis. Clinical manifestations of brain disease often involve imbalances in brain homeostasis and may lead to neurological and behavioral sequelae. This article aims to explore the role of snapin in restoring brain homeostasis after injury or diseases, highlighting its significance in maintaining brain homeostasis and treating brain diseases. Additionally, it comprehensively discusses the implications of snapin in other extracerebral diseases such as diabetes and viral infections, with the objective of determining the clinical potential of snapin in maintaining brain homeostasis.

MicroRNA-361-5p acts as a biomarker for carotid artery stenosis and promotes vascular smooth muscle cell proliferation and migration.

BACKGROUND: Vascular smooth muscle cells (VSMCs) dysfunction participates in carotid artery stenosis (CAS). The study aimed to examine the expression pattern of miR-361-5p in CAS patients, and explore its role in VSMCs proliferation and migration. METHODS: qRT-PCR was performed for the detection of miR-361-5p in serum samples of 150 CAS cases and 150 healthy people. Multiple logistic regression analysis and receiver operating characteristic (ROC) curve was accomplished to detect diagnostic value via SPSS 21.0 statistical software. Cell function of VSMCs was evaluated. Target association was predicted through bioinformatic analysis and confirmed via luciferase activity. RESULTS: Serum miR-361-5p was enhanced in CAS cases and was positively correlated with CAS degree. Logistic regression analysis determined the independent influence of miR-361-5p in CAS, and ROC curve demonstrated its diagnostic value with AUC of 0.892. miR-361-5p promoted VSMCs proliferation and migration, but the influence was counteracted by TIMP4. CONCLUSIONS: MiR-361-5p is a promising biomarker for CAS, and can be used as a potential target for early diagnosis and treatment of CAS. MiR-361-5p can promote VSMCs proliferation and migration via targeting TIMP4.

Silk fibroin carriers with sustained release capacity for treating neurological diseases.

Neurological diseases such as traumatic brain injury, cerebral ischemia, Parkinson's, and Alzheimer's disease usually occur in the central and peripheral nervous system and result in nervous dysfunction, such as cognitive impairment and motor dysfunction. Long-term clinical intervention is necessary for neurological diseases where neural stem cell transplantation has made substantial progress. However, many risks remain for cell therapy, such as puncture bleeding, postoperative infection, low transplantation success rate, and tumor formation. Sustained drug delivery, which aims to maintain the desired steady-state drug concentrations in plasma or local injection sites, is considered as a feasible option to help overcome side effects and improve the therapeutic efficiency of drugs on neurological diseases. Natural polymers such as silk fibroin have excellent biocompatibility, which can be prepared for various end-use material formats, such as microsphere, gel, coating/film, scaffold/conduit, microneedle, and enables the dynamic release of loaded drugs to achieve a desired therapeutic response. Sustained-release drug delivery systems are based on the mechanism of diffusion and degradation by altering the structures of silk fibroin and drugs, factors, and cells, which can induce nerve recovery and restore the function of the nervous system in a slow and persistent manner. Based on these desirable properties of silk fibroin as a carrier with sustained-release capacity, this paper discusses the role of various forms of silk fibroin-based drug delivery materials in treating neurological diseases in recent years.

The Role of Copper Homeostasis in Brain Disease.

In the human body, copper is an important trace element and is a cofactor for several important enzymes involved in energy production, iron metabolism, neuropeptide activation, connective tissue synthesis, and neurotransmitter synthesis. Copper is also necessary for cellular processes, such as the regulation of intracellular signal transduction, catecholamine balance, myelination of neurons, and efficient synaptic transmission in the central nervous system. Copper is naturally present in some foods and is available as a dietary supplement. Only small amounts of copper are typically stored in the body and a large amount of copper is excreted through bile and urine. Given the critical role of copper in a breadth of cellular processes, local concentrations of copper and the cellular distribution of copper transporter proteins in the brain are important to maintain the steady state of the internal environment. The dysfunction of copper metabolism or regulatory pathways results in an imbalance in copper homeostasis in the brain, which can lead to a myriad of acute and chronic pathological effects on neurological function. It suggests a unique mechanism linking copper homeostasis and neuronal activation within the central nervous system. This article explores the relationship between impaired copper homeostasis and neuropathophysiological progress in brain diseases.

[Synthesis and spectral characterization of rare earth complexes of acylpyrazolone-beta-alanine].

In non-aqueous solvent, a new amino-acid schiff base, 1-phenyl-3-methyl-4-benzoyl pyrazolone-5-beta-alanine (HL) was synthesized by a reaction of beta-alanine with benzoylpyrazolone, and its ten rare earth complexes were obtained from refluxing a solution of schiff base and rare earth nitrates. On the basis of elemental analysis and molar conductance, the general formula of the complexes, [REL2NO3] nH2O (RE=La, Sm, Eu, Tb, Y, n=2; RE=Pr, Nd, n = 1; RE=Dy, Er, Yb, n=3), is given. These were characterized by IR, UV-Visible, 1H NMR, 13C NMR and fluorescence. The results show that the schiff base is a tridentate ligand, and the rare earth ions exhibit a coordination of eight in the complexes. In visible spectra, the supersensitive transitions of the Er complex at 522 nm (4 I15/2 -->2 H11/2, 4 S3/2 ) and that of the Nd complex at 573, 584 nm (4I9/2 -->2 G7/2 + 4G5/2) can be observed. Fluorescence of the complexes was produced principally by f-f transition of central ion RE3+, and the ligand has little influence on lightening role. The order of relative intensity of fluorescence of the complexes is ITb > ISm > IEu > IDy.

[Synthesis, spectral characterization and bioactivity of complexes of furoylpyrazolone-thiosemicarbazone].

A new Schiff base containing sulphur, 1-phenyl-3-methyl-4-(alpha-furoyl) pyrazolone-5-thiosemicarbazone (HL) and its Zn(II), Cd(II) and Co(II) complexes have been synthesized. On the basis of elemental analysis and molar conductance, the general formulae of the complexes, [ZnL2] x 1.5H2O, [CdL2] x C2H5OH and [CoL2] x H2O, were given. They were characterized by IR, UV-Visible, 1H NMR, 13C NMR and magnetic moments. The results show that the metal ions exhibit coordination of six in the complexes. The antibacterial experiments indicate that they have high antibacterial activities against S. aureus, B. subtilis, E. coli, E. carotovora, and C. flaccumfaciens.

[Synthesis and spectral characterization of boron complexes of bis-schiff base from acylpyrazolone].

Three novel bis-schiff base complexes [B(PMaFP)2en]Ac, [B(PMaFP)2pen]Ac and [B(PMTHP)2en]Ac have been synthesized, where (HPMalphaFP)2 en = N,N'-bis [(1-phenyl-3-methyl-5-oxo-4-pyrazolinyl) alpha-furylmethylidyne] ethylenediimine, (HPMalphaFP)2pen = N,N'-bis[(1-phenyl-3-methyl-5-oxo-4-pyrazolinyl) alpha-furylmethylidyne]-o-phenylenediimine and (HPMTHP)2en = N,N'-bis[(1-phenyl-3-methyl-5-oxo-4-pyrazolinyl)-2-thenoylmethylidyne] ethylenediimine. They were characterized by elemental analysis, IR, UV-Vis, 1H NMR, 13C NMR, and molar conductance measurements. The results show that the bis-schiff base is a quadridentate ligand and boron is four-coordinated in the complexes.

[Synthesis and spectral characterization of U(VI) and Th(IV) complexes of thenoylpyrazolone-ethylenediamine].

Two novel bis-schiff base complexes [UO2 (PMTHP)2en] and [Th(PMTHP)2en(NO3)2] have been synthesized, where (PMTHP)2en = N,N'-bis[(1-phenyl-3-methyl-5-oxo-5-pyrazolinyl)- 2-thenoylmethylidyne] ethylenediamine, and characterized by elemental analysis, IR, UV-Vis, 1H NMR, 13C NMR and molar conductance measurements. The results show that the bis-schiff base is a quadridentate ligand and the nitrate a bidentate ligand, and the uranyl and thorium ions exhibit coordination of six and eight in the complexes, respectively.