Senescent microglia: The hidden culprits accelerating Alzheimer's disease.

Ageing is a major risk factor for neurodegenerative diseases like Alzheimer's disease (AD). Microglia, as the principal innate immune cells within the brain, exert homeostatic and active immunological defense functions throughout human lifespan. The age-related dysfunction of microglia is currently recognized as a pivotal trigger for brain diseases associated with aging.

Tinosinenside A inhibits neuroinflammation and protects HT22 cells by suppressing the TLR4/NF-κB/NLRP3 signaling pathway in BV2 cells.

Microglia-mediated neuroinflammation plays a crucial role in Alzheimer's disease (AD). Tinosinenside A (Tis A) is a novel sesquiterpene glycoside isolated from the dried rattan stem of Tinospora sinensis (Lour.) Merr.

Erjingpill bionic cerebrospinal fluid alleviates LPS-induced inflammatory response in BV2 cells by inhibiting glycolysis via mTOR.

Ethnopharmacological Relevance: Erjingpill, a well-known prescription documented in the classic Chinese medical text "Shengji Zonglu," has been proven to have effective alleviating effects on neuroinflammation in Alzheimer's disease (AD). Although the alterations in microglial cell glycolysis are known to play a crucial role in the development of neuroinflammation, it remains unclear whether the anti-neuroinflammatory effects of Erjingpill are associated with its impact on microglial cell glycolysis.

Aim Of The Study: This study aims to determine whether Erjingpill exerts anti-neuroinflammatory effects by influencing microglial cell glycolysis.

Pharmacokinetic-Pharmacodynamic Correlation Analysis of in Rats with Myocardial Ischemia.

The pharmacokinetics (PK) of in rats were studied, and pharmacokinetic-pharmacodynamic (PK-PD) correlation analysis was performed to elucidate their time-concentration-effect relationship. The myocardial ischemia model was made with pituitrin. Rats were divided into sham operation, sham operation administration, model, and model administration groups (SG, SDG, MG, and MDG, respectively; = 6).

[Effect of Erjing Pills on alleviating neuroinflammation of AD rats based on TLR4/NF-κB/NLRP3 pathway and its mechanism].

This paper aimed to study the effect of Erjing Pills on the improvement of neuroinflammation of rats with Alzheimer's di-sease(AD) induced by the combination of D-galactose and Aβ_(25-35) and its mechanism. SD rats were randomly divided into a sham group, a model control group, a positive drug group(donepezil, 1 mg·kg~(-1)), an Erjing Pills high-dose group(9.0 g·kg~(-1)), and an Erjing Pills low-dose group(4.

Research on the Material Basis and Mechanism of Kudzu Root in Preventing and Treating Cerebral Ischemia based on Network Pharmacology.

Background: It has been shown that Kudzu root has significant pharmacological effects such as improving microcirculation, dilating coronary arteries, and increasing cerebral and coronary blood flow, but its material basis and mechanism of action are not clear.

Objective: The aim of this study was to investigate the mechanism of action of Kudzu root in the prevention and treatment of cerebral ischemia (CI) through network pharmacology combined with animal experiments.

Methods: The components of kudzu root were screened by using the Chemistry Database, Chinese Academy of Science.

Nuciferine attenuates acute ischemic stroke in a rat model: a metabolomic approach for the mechanistic study.

Lotus leaves have the dual identity of medicine and food homology as included in the Chinese Pharmacopoeia. Nuciferine is the major bioactive component which is highly abundant in the leaves of . Nuciferine has been shown to potentially improve energy metabolism and protect neurons in cerebral ischemia.

Protective effects of 5(S)-5-carboxystrictosidine on myocardial ischemia-reperfusion injury through activation of mitochondrial KATP channels.

5(S)-5-carboxystrictosidine (5-CS) is a compound found in Mappianthus iodoides Hand.-Mazz., root, a traditional Chinese medicine used for the treatment of coronary artery disease.

Erzhi pills ameliorate cognitive dysfunction and alter proteomic hippocampus profiles induced by d-galactose and Aβ injection in ovariectomized Alzheimer's disease model rats.

Context: Erzhi pills are a classic Chinese medicine prescription, but their effects on Alzheimer's disease (AD) are not clear.

Objective: The protective effects of Erzhi pills in AD rats and their potential mechanisms were investigated.

Materials And Methods: An AD rat model was established by ovariectomy combined with d-galactose and Aβ injection.

Evidence-based complementary and alternative medicine bioinformatics approach through network pharmacology and molecular docking to determine the molecular mechanisms of Erjing pill in Alzheimer's disease.

Erjing pill, a Traditional Chinese Medicine (TCM) formulation composed of and , has an important role in the treatment of Alzheimer's disease (AD). However, the underlying mechanisms of the action of Erjing pill in AD have remained elusive. In the present study, the key ingredients of Erjing pill were investigated and the active components and their mechanisms of action on AD were analyzed based on networks pharmacology.

α-Hederin inhibits the growth of lung cancer A549 cells and by decreasing SIRT6 dependent glycolysis.

Context: α-Hederin, a potent bioactive compound of (Bunge) Regel (Ranunculaceae), has many pharmacological uses, but its effect on cancer cell metabolism is still unclear.

Objective: To elucidate the role of α-hederin in the glucose metabolism of lung cancer cells.

Materials And Methods: Cell Counting Kit 8 and colony formation assays were employed to assess the antiproliferative effects of α-hederin.

Epigallocatechin gallate reduces uric acid levels by regulating xanthine oxidase activity and uric acid excretion in vitro and in vivo.

Background: This study investigates the effect of epigallocatechin gallate (EGCG) from tea leaves on hyperuricemia and explores the underlying mechanisms in vitro and in vivo.

Methods: The effects of EGCG on proliferation of BRL 3A rat liver cells were evaluated by CCK8 and after stimulation by xanthine the uric acid and xanthine oxidase (XOD) levels were evaluated by a kit; In an in vivo experiment, rats were treated with oxonic acid potassium salt combined with ethylamine pyrimidine to induce high uric acid hematic disease (7 days), The serum uric acid levels and XOD levels were evaluated by a kit, The expressions of OTA1 and GLUT9 were detected by RT-qPCR and Immunohistochemical.

Results: EGCG had no effect on proliferation, and significantly reduced serum uric acid levels and inhibited XOD activity (P<0.

Molecular mechanistic insight into the anti-hyperuricemic effect of Eucommia ulmoides in mice and rats.

Context: Eucommia ulmoides Oliver (Eucommiaceae) has various medicinal properties. Our previous studies revealed that Eucommia ulmoides has a protective effect on hyperuricaemia.

Objective: This study investigates the effect of Eucommia ulmoides cortex ethanol extract (EU) on hyperuricaemia and explores the underlying mechanism in Kunming mice and Sprague-Dawley rats.

Resveratrol protects cardiomyocytes against anoxia/reoxygenation via dephosphorylation of VDAC1 by Akt-GSK3 β pathway.

Our previous studies showed that the effect of resveratrol preventing mitochondrial permeability transition pore (mPTP) opening in myocardial ischemia/reperfusion injury was achieved by regulating voltage-dependent anion channel 1 (VDAC1). However, the underlying mechanism remains unclear. Previous studies demonstrated that the activity and function of VDAC1 are highly regulated by post-translational modification.

VDAC1 deacetylation is involved in the protective effects of resveratrol against mitochondria-mediated apoptosis in cardiomyocytes subjected to anoxia/reoxygenation injury.

We have recently demonstrated that Voltage-dependent anion channel 1 (VDAC1), a protein located in the mitochondrial outer membrane, is involved in the effects of resveratrol on the mitochondrial permeability transition pore (mPTP). However, the underlying mechanism of action remains to be elucidated. In the present study, we demonstrated that resveratrol promoted VDAC1 deacetylation in cardiomyocytes in response to anoxia/reoxygenation (A/R) injury.