Objective This study aims to explore whether Loureirin A can mitigate neutrophil-related pathology and vascular damage in a photothrombotic stroke model.Methods C57BL/6J mice were divided into three groups:sham-operated,model,and Loureirin A administered(Model+Loureirin A,10 mg·kg-1).A mouse model of focal cerebral ischemia was established using photothrombosis(PT),and the administration of Loureirin A commenced one day post-surgery via intraperitoneal injection for three consecutive days.Neurological function was assessed in the mice 24 h post-PT modeling,while the infarction rate was evaluated through TTC staining three days post-PT modeling.MPO-positive cell infiltration in the peri-infarct cortex was detected by immunohistochemistry.The reactive oxygen species(ROS)content was observed via immunofluorescence staining.Cerebral blood flow in mice was measured by laser speckle imaging.The expression of tight junction proteins ZO-1(Zonula occludens-1),Occludin,and matrix metalloproteinase-9(MMP-9)was detected by immunoblotting.Vascular permeability was assessed by 40 kDa FITC-Dextran,and peri-infarct vascular density was detected by 2000 kDa FITC-Dextran.Results Loureirin A markedly decreased the cerebral infarction rate and the extent of neurological functional impairment,and enhancing blood perfusion.Pathological examinations revealed that Loureirin A lessened neutrophil infiltration,reduced intracellular ROS,and increased the protein expression of ZO-1 and Occludin,which are critical components of the blood-brain barrier.Concurrently,it downregulated Matrix Metalloproteinase-9(MMP-9).Furthermore,Loureirin A diminished the leakage of extracellular 40 kDa dextran,bolstered peri-infarct cerebral vascular perfusion,and mitigated vascular injury.Conclusion Loureirin A can inhibit neutrophil infiltration and vascular injury after cerebral ischemia.

Objective This study aims to explore whether Loureirin A can mitigate neutrophil-related pathology and vascular damage in a photothrombotic stroke model.Methods C57BL/6J mice were divided into three groups:sham-operated,model,and Loureirin A administered(Model+Loureirin A,10 mg·kg-1).A mouse model of focal cerebral ischemia was established using photothrombosis(PT),and the administration of Loureirin A commenced one day post-surgery via intraperitoneal injection for three consecutive days.Neurological function was assessed in the mice 24 h post-PT modeling,while the infarction rate was evaluated through TTC staining three days post-PT modeling.MPO-positive cell infiltration in the peri-infarct cortex was detected by immunohistochemistry.The reactive oxygen species(ROS)content was observed via immunofluorescence staining.Cerebral blood flow in mice was measured by laser speckle imaging.The expression of tight junction proteins ZO-1(Zonula occludens-1),Occludin,and matrix metalloproteinase-9(MMP-9)was detected by immunoblotting.Vascular permeability was assessed by 40 kDa FITC-Dextran,and peri-infarct vascular density was detected by 2000 kDa FITC-Dextran.Results Loureirin A markedly decreased the cerebral infarction rate and the extent of neurological functional impairment,and enhancing blood perfusion.Pathological examinations revealed that Loureirin A lessened neutrophil infiltration,reduced intracellular ROS,and increased the protein expression of ZO-1 and Occludin,which are critical components of the blood-brain barrier.Concurrently,it downregulated Matrix Metalloproteinase-9(MMP-9).Furthermore,Loureirin A diminished the leakage of extracellular 40 kDa dextran,bolstered peri-infarct cerebral vascular perfusion,and mitigated vascular injury.Conclusion Loureirin A can inhibit neutrophil infiltration and vascular injury after cerebral ischemia.

Depression is a common psychiatric disorder characterized by a wide range of clinical manifestations, including depressed mood, psychomotor retardation, diminished motivation, anhedonia, despair, and even suicidality. The heterogeneity of the features of depression indicates the diversity of its pathogenesis. Protein levels and their genetic abnormalities are essential factors in the pathogenesis of depression. This review focuses on the levels and genetic abnormalities of depression-related proteins to further elaborate the pathogenesis of depression and presents current problems and challenges to provide a theoretical foundation for the development of novel antidepressant medications.

The EtOH extracts of the whole plants of afforded 17 new jatrophane diterpenoid esters, helioscopianoids A-Q (-), along with eight known compounds (-). Their structures were elucidated by extensive spectroscopic methods and Mo(OAc)-induced ECD analysis, and the structures of compounds , , and were confirmed by X-ray crystallography. Compounds - were evaluated for inhibitory effects on P-glycoprotein (P-gp) in an adriamycin (ADM)-resistant human breast adenocarcinoma cell line (MCF-7/ADR) and neuroprotective effects against serum deprivation-induced and rotenone-induced PC12 cell damage. Compounds and increased the accumulation of ADM in MCF-7/ADR cells by approximately 3-fold at a concentration of 20 μmol/L. Compound could attenuate rotenone-induced PC12 cell damage, and compounds , , and showed neuroprotective activities against serum deprivation-induced PC12 cell damage.

Aim To research the synergistic effect of hyperlipoproteinemia and Aβ in the processing of Alzheimer′s disease.Methods Seventy SD rats were randomly divided into seven groups, and dealt with D-gal(hypodermic injection), hyperlipemia diet, microinjection into both side of CA1 section in hippocampus, independently.Morris water maze(MWM) test was used to evaluate the spatial memory impairments.Tau and tau(pThr181) pathology in the hippocampus were detected using Western blot and immunohistochemistry.Nissl′s staining was used to detect cell apoptosis.Results Aβ25-35-treated rats showed significant impairments of spatial memory in MWM test, especially in the group of D-gal+Aβ25-35+HLD(P<0.01).Furthermore, these rats treated with Aβ25-35, D-gal, and hyperlipemia diet, exhibited significantly increased phosphorylation of tau, particularly in the Thr181 site.Conclusion Hyperlipoproteinemia is the risk factor for older person, which could strengthen the toxic effect of Aβ, and promote phosphorylation of tau.

Chemokines play pleiotropic roles in the pathology of Alzheimer′s disease(AD),a chronic inflammatory disease of central nervous system.The neuropathological features of AD include neurofibrillary tangles,amyloid plaques,neuroinflammation,and neuronal synaptic loss.Chemokines are involved in the pathogenesis of AD by activating or regulating inflammatory cells or glial cells,playing dual key roles of the pro-and anti-inflammatory properties in AD.The levels of chemokines in serum,cerebrospinal fluid and brain tissue of AD patients are changed accordingly.This review summarizes the role of chemokines and their receptors in AD in the biological activities and unveils the changing rules,aiming to provide new strategies for clinical treatment of AD.

Since Parkin was confirmed by the Japanese scholar to be associated with juvenile Parkinson′s disease, it has come to be the focus of the scholars and a lot of researches have been made on it. Apart from Parkinson′s disease, many other disea-ses have also been proved to be associated with the role of Parkin and its interaction with protein substrates, especially in various kinds of cancer diseases and leukemia. This paper focuses on the latest research about Parkin and its development in tumor diseases and leukemia.

Chemokine is a small protein which plays an impor-tant role in men's physiological function.It has chemotactic ac-tivity and is often secreted by immune cells and glial cells like microglia or astrocytes.Through the effect of chemokine recep-tors on target cells,various immune cells can achieve directional migration and play an important role in the diseases related with immunity and inflammation.CCL2,also known as monocyte chemotactic protein-1 (MCP-1 ),is one member of chemokine CC subfamily (βsubfamily).It can chemokine monocytes, macrophages and T lymphocytes to affect their phagocytosis func-tion and produce antibodies to combat invading microorganisms. In recent years,it has been found that CCL2 plays a key role in the occurrence and development of the problems concerning cen-tral nervous system and immune system as well as cancer, AIDS,leukemia,diabetes and other diseases.This thesis is to give an elaboration on the latest research on CCL2 and the rele-vant diseases.

Discovery of noncoding RNA(ncRNA)over the past decade has reflected a paradigm shift of traditional RNA research. There is evidence that RNA can function not only as a messenger between DNA and protein,but as a regulator of genome organization and gene expression,which is increasingly elaborate in complex organisms. ncRNA seems to operate at many levels,however,in?cluding the physiological and pathological status. The research of ncRNA in pharmacology has not been summarized before. Here,we reviewed the emergence of the ncRNA in the research of pharma? cology,such as acting as biomarkers and medical targets. Besides,we mentioned their role in drug resistance and drug addiction in order to highlight the significant role of ncRNA in pharmacology.

Aim To the investigate the protective effect of ginsenoside Rg1 in Alzheimer's disease ( AD)-like neurotoxicity model induced by okadaic acid ( OKA) in the cellular level , and explore the mecha-nism preliminarily. Methods The PC12 cells model, simulate neurons, induced by OKA was given Rg1 (1, 5,10 μmol·L-1), and melatonin (Melat) 10 μmol· L-1 was given as a positive control. MTT and LDH were carried out to assess the cell viability and mortality. To detect the accumulation of ROS, the DCFH-DA fluores-cent probe was conducted. And to assess the change of the activity of a variety of antioxidant enzymes, various kits were used, including ABTS、CAT、SOD、GSH-Px and GSSG/GSH. Results Compared with the control group, the survival rate of PC12 cell in OKA group re-duces significantly, the mortality rate was increased sig-nificantly , the number of early apoptotic cells was in-creased significantly (P<0. 01). Oxidative stress-relat-ed indicators show that ROS accumulation within the cells of OKA group increases significantly ( P<0. 01 ) , and the total antioxidant capacity ( ABTS ) decreases significantly ( P < 0. 01 ) , the activity of peroxidase (Catalase, CAT) (P <0. 01), glutathione peroxidase (glutathione peroxidase, GSH-Px) and superoxide dis-mutase ( superoxide dismutase, SOD) decreased signifi-cantly ( P <0. 05 ) , the rate of GSSG/GSH increased significantly ( P <0. 01 ) . Compared with the model group, the different doses of Rg1 could improve the sur-vival rate and decrease the mortality rate of PC12 cell significantly in the group of OKA, and could decrease the level of the accumulation of ROS, improve the activ-ity of antioxidant enzymes. Conclusion Ginsenoside Rg1 can decrease PC12 cell apoptosis by exerting an-tioxidant effects, and protect the nerve cells in AD-like pathology model induced by OKA.