Abstract: Objective To investigate apoptosis after PDCD2 overexpression in Jurkat and ACH2 cell lines. Methods Jurkat and ACH2 cell lines were used in this study. PDCD2 was stably expressed in the cell lines by lentivirus infection. Apoptosis was determined by flow cytometry after 24 hours of TRAIL treatment. Results Apoptosis was not significantly increased in Jurkat or ACH2 cells stably expressing PDCD2 compared with untransfected control cells. However, compared with the control group without PDCD2 overexpression, apoptosis was significantly higher in PDCD2- Jurkat and PDCD2-ACH2 cells induced by TRAIL (P< 0.05). Conclusions PDCD2 promotes apoptosis of T cell and HIV latent-infected T cells induced by TRAIL.

Abstract: Objective To establish Sdpr-gene-knockout and Sdpr transgenic mouse models to provide suitable models for studying Sdpr gene function. Methods Sdpr-knockout mice were constructed by CRISPR/ Cas9 technology, while Sdpr transgenic mice were constructed using plasmid overexpression. We identified mouse genotypes by PCR. The mRNA and protein expression levels were determined by qRT-PCR and Western blot. Mouse tissues were obtained for histopathological analysis. We analyzed the immune cells of the knockout mice and transgenic mice by flow cytometry. Results Sdpr-gene-knockout and transgenic mouse models were obtained. Compared with that in the wild-type mice, the Sdpr gene expression level was decreased in the knockout mice. Meanwhile, inflammatory foci appeared in many tissues, such as inflammatory cells infiltrated into the lungs and fat. Hepatic steatosis can be observed, and extramedullary hematopoiesis can be seen around the central hepatic vein. Extramedullary hematopoiesis can be observed in the red pulp of the spleen. The proportion of T cells in bone marrow of the knockout mice decreased, the number of CD4^-CD8^- T cells in the thymus increased, while CD4⁺CD8⁺ T cells decreased. In terms of the findings in the transgenic mice, the expression level of the Sdpr gene increased. In addition, their liver cells showed slight fatty degeneration and widening of alveolar septa. Moreover, spleen lymphocytes exhibited hyperplasia and red pulp cells increased. The proportion of B cells in the peripheral blood of the transgenic mice increased while the proportions of myeloid and T cells decreased. Finally, thymus CD4⁺ T cells increased while CD4⁺ CD8⁺ T cells decreased. Conclusions Sdpr-knockout and transgenic mice were successfully established and identified, which can provide models for studying the mechanisms of action of Sdpr protein and its related caveolin protein in different tissues and organs.

Abstract: Objective To investigate the effect of estrogen deficiency on the degeneration of spinal endplate chondrocytes. Methods Forty 6-month-old rats were divided into ovariectomy (OVX) and sham operation groups. All of the rats were sacrificed at week 9 after operation. The cartilage endplate tissue was extracted, and endplate chondrocytes were cultured. The expression of COL-II in the cartilage endplate tissue was evaluated by immunohistochemistry. The cells were stained by toluidine blue to identify endplate chondrocytes. The viability of endplate chondrocytes was detected by CCK-8. Fluorescence staining of rhodamine-labeled phalloidin was used to observe the changes of F-actin after OVX. Cellular immunofluorescence was performed to detect the changes of COL-II of endplate chondrocytes. The expression levels of SOX9, ACAN, ADAMTS-5, MMP13 and COL-X were compared between the two groups by RT-qPCR. Results After OVX, the expression of COL-II protein in the cartilage endplates was decreased. Most of the chondrocytes in the endplates were polygonal and fusiform, arranged like paving stones. Endplate chondrocytes of OVX demonstrated more disordered cytoskeleton, decreased viability, increased stress fibers, decreased migration ability, and lower COL-II expression. For the OVX group, the expression of SOX9 and ACAN in the endplate chondrocytes was decreased, while that of ADAMTS-5, MMP13 and COL-X was increased. Conclusions Estrogen deficiency can cause degeneration of endplate chondrocytes.

Abstract: Objective To investigate the reactivation effect of nicotinamide (NAM) on latent virus in SIV/ SHIV- infected monkey CD4⁺T cells. Methods Peripheral blood from five SIV/ SHIV-infected rhesus monkeys was collected with undetectable virus loads for at least half a year. CD4⁺ T cells were sorted and treated with latency-reversing agents accompanied by monitoring of viral loads in supernatants and changes in activated T cell surface markers and coreceptors CXCR4 and CCR5 on CD4⁺T cells. Changes in nuclear antigen SIRT1 were detected by Western blot. Results NAM had a good activation effect on latent virus in SIV/ SHIV-infected monkey CD4⁺T cells and reached a higher level combined with GS-9620. This did not cause extensive activation of T cells and had no influence on CCR5 expression, while CXCR4 expression was slightly upregulated. NAM significantly reduced expression of nuclear antigen SIRT1. Conclusions NAM is a good choice for a latency-reversing agent.

Abstract: Objective To investigate the effect of the amyloid beta precursor protein binding protein B1 (Apbb1) gene on H9c2 cardiomyocyte proliferation and its potential mechanism. Methods H9c2 cardiomyocytes were treated with small interfering RNA and pcDNA3. 1⁺ plasmid for knockdown and overexpression of the Apbb1 gene, and cell proliferation was detected by CCK8, qPCR and immunofluorescence assay, to evaluate the effect of this gene on cardiomyocyte proliferation. Next, the proteins interacting with the Apbb1 protein were analyzed using the online database String to explore how Apbb1 might function. In the experiment, four groups were established: knockdown control group, Apbb1- knockdown group, overexpression control group and Apbb1-overexpression group. Results Compared with that in the knockdown control group, expression of the Apbb1 gene in the Apbb1-knockdown group decreased by 52% (P<0.05, n= 3) and cell proliferation decreased by 44% at 48 h (P<0.01, n= 3), but cell proliferation increased by 86% at 72 h (P< 0.0001, n= 3). The expression levels of Ccnb1 and Ccna2 mRNA were increased by 80% (P<0.001, n= 3) and 76% (P<0.001, n= 3), respectively. Immunofluorescence assay showed that PH3- and Aurora B-positive cells increased by 4. 33% (P< 0.01, n= 3) and 4. 67% (P< 0.05, n= 3). Compared with that in the overexpression control group, the expression of the Apbb1 gene was upregulated 119-fold in the Apbb1-overexpression group (P<0.0001, n= 3), and cell proliferation decreased by 1. 23 times at 48 h (P< 0.0001, n= 3) and 1. 04 times at 72 h ( P< 0.0001, n= 3). The expression levels of Ki67, a marker of cell proliferation, and Ccnb1 and Ccna2 mRNA encoded by cell cycle-related genes were decreased by 25% ( P< 0.01, n= 3), 72% ( P< 0.001, n= 3), and 38% ( P< 0.001, n= 3), respectively. Meanwhile, PH3- and Aurora B-positive cells decreased by 3. 7% (P< 0.01, n= 3) and 4. 36% (P< 0.05, n= 3), respectively. The result of protein interaction network analysis showed that KAT5, APP and APLP2 were the proteins that most significantly interacted with Apbb1. Conclusions Knockdown of the Apbb1 gene promotes the proliferation of H9c2 cardiomyocytes, while its overexpression inhibits their proliferation. Apbb1 may affect the proliferation of cardiomyocytes by influencing the G2 / M phase of the cell cycle and KAT5 may interact with Apbb1 protein to affect cardiomyocyte proliferation .

Abstract: Objective To investigate the inhibitory effect of gambogic acid (GA) on the growth of prostate cancer (PCa) cells representing different clinical characteristics. Methods The androgen-dependent PCa cells LNCaP, androgen-resistant PCa cells 22RV1, and neuroendocrine PCa cells PC3 were treated with GA and enzalutamide (Enz). IC₅₀ values of the treated cells were determined by the CCK8 method . The expression levels of androgen receptor (AR), Ki67, Cleaved caspase-3 and Bcl-2 and the apoptosis of the different PCa cells treated with GA were determined by qRT- PCR, Western blot and flow cytometry. PC3 cells were implanted subcutaneously into male nude mice, and then the tumor- bearing mice were divided into three groups at random: Control group, Enz group and GA group. The changes of tumor volume were measured during drug treatment, and the tumor weight was determined after treatment to evaluate the overall effect of drug treatment. Results Compared with Enz, GA displayed achieved better inhibitory effection for of the growth of LNCaP, 22RV1 and PC3 cells, and a lower dose of GA can could reduce the proliferation and activity of these cells. Under the effect of GA, the expression of Ki67 and AR in PCa cells was significantly decreased (P<0.05). With increasing GA concentration, the number of apoptotic PCa cells gradually increased, and the expression of apoptosis-related protein Cleaved caspase-3 increased (P<0.001) and that of bcl-2 decreased (P< 0.001). In vivo, compared with those in the Control group, tumor volume and weight decreased in the Enz group, albeit not significantly, while tumor volume and weight decreased significantly in the GA group (P<0.01). Conclusions GA can inhibit the growth of PCa cells in vivo and in vitro, as well as the expression of AR and Ki67 in these cells. GA can also promote the apoptosis of tumor cells by regulating the expression of Cleaved caspase-3 and Bcl-2 proteins.

Abstract: Objective To study the effects of xi-xian-tong-shuan capsules on chronic cerebral hypoperfusion rats. Methods A rat model of chronic cerebral hypoperfusion was established by ligating bilateral common carotid arteries, and then xi-xian-tong-shuan capsules were given daily for 42 days. Water maze test was used to evaluate the learning and cognitive functions of these rats. Neurons in the hippocampus were observed by Nissl’ s staining and blood brain barrier (BBB) function was evaluated by immunofluorescence staining. BBB-related proteins in plasma and brain tissues were detected by ELISA and Western blot, respectively. Results Xi-xian-tong-shuan capsules ameliorated the declines of learning and cognitive functions in rats after chronic cerebral hypoperfusion, reduced the number of Nissl bodies and amount of IgG leakage in the hippocampus, and enhanced the expression of BBB-related proteins, when compared with those in the model group. Conclusions Xi-xian-tong-shuan capsules improved learning and cognitive functions after chronic cerebral ischemia by alleviating the damage to the BBB.

Abstract: Objective To investigate the role of the endoplasmic reticulum (ER) stress-mitochondrial autophagy pathway in pulmonary arterial hypertension ( PAH) in rats by inhibiting ER stress induced by monocrotaline. Methods SD rats were randomly divided into three groups (15 rats per group): normal control group, group with PAH induced by monocrotaline, and 4-phenylbutyric acid (4-PBA) group. The mean pulmonary artery pressure (mPAP) and mean right ventricular pressure (mRVP) in the rats were measured by the Biological Information Acquisition System. The remodeling of pulmonary vessels was observed by hematoxylin-eosin (HE) staining, while ImageJ was used to measure indices related to pulmonary vascular remodeling. The ultrastructure of mitochondria in pulmonary artery smooth muscle cells was observed by electron microscopy. Quantitative real-time PCR analysis was used to measure the mRNA levels of the key factors in the ER stress-mitochondrial autophagy pathway. Results (1) mPAP and mRVP increased in the PAH group (P<0.001). However, after 4-PBA intervention, mPAP and mRVP decreased compared with those in the PAH group (P<0.001). (2) HE staining showed clear remodeling of pulmonary small vessels in the PAH group, and the measurement of vascular remodeling indices indicated increased thickness of pulmonary arteriole media and lumen stenosis (P< 0.05). ( 3) The mitochondria of pulmonary artery smooth muscle cells in the PAH group were swollen, the mitochondrial crista structure had dissolved or disappeared, and mitochondrial autophagy was increased, as revealed by electron microscopy. After the ES stress was inhibited, destruction of the mitochondrial structure and mitochondrial autophagy were reduced. (4) Compared with those in the NC group, the mRNA expression levels of ERS-related factors PERK, ATF4, Bcl-2 and CHOP were increased in the PAH group (P<0.001), mitochondrial fusion factor Mfn2 decreased (P<0.001), mitochondrial fission factor Drp1 increased (P<0.001), and the expression of Atg12, LC3 and p62 increased in the PAH group (P<0.001). After rats had been administered 4-PBA, the mRNA expression levels of ERS-related factors decreased (P<0.001), the mRNA level of Mfn2 increased (P<0.001), while that of Drp1 decreased (P<0.001). Moreover, the mRNA expression levels of mitochondrial autophagy factors Atg12, LC3 and P62 (P<0.01) decreased. Conclusions ERS may promote the establishment and progression of pulmonary hypertension through the mitochondrial autophagy pathway. This may provide a new concept for the treatment and prevention of pulmonary hypertension.

Abstract: Objective To explore the effect of naringenin on the insulin resistance of 3T3-L1 adipocytes, and the relationship between the overexpression of miR-29b and the effects of naringenin on insulin resistance in 3T3-L1 adipocytes, in order to further illustrate the mechanism by which naringenin acts in the prevention and treatment of T2DM. Methods Dexamethasone was used to induce differentiated and mature 3T3-L1 adipocytes, after which an insulin resistance (IR) model was established. Different concentrations of naringenin were used to intervene in IR model cells and IR models cells transfected with miR-29b mimics and inhibitor. qRT-PCR and Western blot were used to determine the gene and protein expression of IRS-1, Akt / p-Akt and GLUT4. Results Naringenin intervention increased the gene and protein expression of IRS-1, Akt / p-Akt and GLUT4 that was reduced in 3T3-L1 IR model cells. Naringenin increased 3T3-L1 IR model cell IRS-1, Akt / p-Akt and GLUT4 gene and protein expression by inhibiting the overexpression of miR-29b. Conclusions These result show that naringenin can ameliorate insulin resistance in 3T3-L1 adipocytes, which may improve the expression of related proteins in the PI3K/ Akt signaling pathway by inhibiting the high expression of miR-29b.

Abstract: Objective To explore the mechanism by which oridonin regulates the microRNA200c (miR-200c) / enhancer of zeste homolog 2 (EZH2) axis to inhibit the epithelial-mesenchymal transition (EMT) of melanoma cells (A375 cells). Methods The MTT method was used to detect the effect of Rubescensine A on the viability of A375 cells. A375 cells were divided into a control group, oridonin group, mimic control group, miR-200c mimic group, oridonin+inhibitor control group, and oridonin+miR-200c inhibitor group. qRT-PCR was used to detect the expression of miR-200c and EZH2 mRNA, Western blot was used to detect the expression of EZH2 and EMT-related proteins, adhesion test was used to detect the adhesiveness of A375 cells, Transwell test was used to detect the invasiveness and migration abilities of A375 cells, while a luciferase reporter gene experiment was used to detect the targeting relationship between miR-200c and EZH2, construct a nude mouse model of transplanted tumor to detect tumor quality. Finally, the expression of EMT-related proteins was analyzed immunohistochemically. Results The survival rate of A375 cells decreased significantly with increasing oridonin concentration in a dose-dependent manner (P<0.05). Since 40 μmol / L oridonin was close to the half inhibitory concentration, 40 μmol / L oridonin was selected for follow-up experiments. Compared with those in the control group, the expression levels of miR-200c and E-cadherin in A375 cells in the oridonin group and miR-200c mimic group increased significantly, while the expression levels of EZH2 mRNA and protein, neural cadherin ( N-cadherin), and Vimentin, number of migrating cells, number of invading cells, and number of adhering cells decreased significantly ( P< 0.05). Compared with the control group and the mimic control group, the expression level of EZH2 protein in the miR-200c mimics group was significantly decreased (P<0. 05), and the silencing of miR-200c could reverse the effect of oridonin on A375 cells. Compared with the levels in the control group, the tumor quality and expression levels of EZH2 mRNA, N-cadherin, and Vimentin were significantly decreased in the oridonin group, while the expression levels of miR-200c and E-cadherin were significantly increased ( P< 0.05). Moreover, compared with those in the oridonin group, the tumor quality and expression levels of EZH2 mRNA, N-cadherin and Vimentin in the oridonin+miR-200c inhibitor group were significantly increased, while the expression levels of miR-200c and E-cadherin were significantly decreased (P<0.05). Conclusions Oridonin may inhibit the EMT of A375 cells and tumor growth by promoting the miR-200c / EZH2 axis.

Abstract: Objective To investigate the safety and efficacy of human umbilical cord mesenchymal stem cells (HUC-MSCs) in treating lipopolysaccharide (LPS) induced acute lung injury in a mouse model. Methods The safety of HUC-MSCs was evaluated through tumorigenicity experiments, in vitro hemolysis experiments, and acute toxicity experiments. A model of acute lung injury was constructed by nasal or intraperitoneal injection of LPS in mice aged 6 to 8 weeks. HUC-MSCs treatment was given 6 h after modeling, and the treatment groups were divided into tail vein injection group (5×10⁷ cells/ kg) and nebulized group (HUC-MSCs conditioned medium). The histopathological result of mice lungs in each group were observed 96 h after modeling, and the inflammatory cell count and classification of bronchoalveolar lavage fluid ( BALF ) were observed by Richter-Kimsa staining. Results There was the absence of potentially tumorigenicity and acute toxicity in the animals after administration of the stem cells.HUC-MSCs had no hemolytic effect on rabbit blood. Compared with the control group, both modeling method showed some degree of lung injury, and the McGuigan score of lung histopathological sections showed that the lung injury caused by intraperitoneal injection of LPS was more severe than that of the nasal drip group. Compared with the model group, the degree of lung injury was significantly reduced in the treatment group, in which the tail vein injection group had a better treatment effect than the atomization group, and the macrophage count in BALF was significantly higher (P<0.001). Conclusions The mouse model of acute lung injury induced by LPS intraperitoneal injection was superior to nasal drip administration. Caudal vein injection of HUC- MSCs can effectively treat acute lung injury in mice. HUC-MSCs conditioned medium atomization can alleviate lung inflammation in mice.

Abstract: Objective To observe the effects of different doses of protease inhibitor I (PSI) on behavior and the expression of tyrosine hydroxylase ( TH) and α-synuclein in the substantia nigra of rats, and to explore the optimal conditions for establishing a chronic Parkinson’s disease (PD) rat model induced by PSI. Methods Thirty SPF male rats were randomly and equally divided into three groups. Model groups were subcutaneously injected with PSI at a dose of 3 or 6 mg / kg, while the control group was injected with dimethyl sulfoxide solution at a dose of 3 mg / kg. After injection every other day (every Monday, Wednesday and Friday) for 2 weeks, the behavioral changes of PD rats were observed, and the changes of cells in the substantia nigra of the midbrain were observed by routine HE staining. The expression of TH and α- syn in the substantia nigra of dopaminergic neurons was determined by western blotting and immunohistochemical staining. Results Compared with that in the control group, the motor ability of the rats in the PSI model group was significantly decreased, the behavioral score in the pole climbing test was lower in the 3 mg / kg dose group than that in the 6 mg / kg dose group, and the behavioral score in the suspension test was higher in the 3 mg / kg dose group than that in the 6 mg / kg dose group. The result of HE staining showed that the substantia nigra cells of the model group were degenerated. The result of Western blot and immunohistochemistry showed that the expression of TH decreased significantly and that of α-syn increased significantly in the substantia nigra of rats. Conclusions The PSI rat model can replicate the behavioral and central and peripheral neurodegenerative changes of PD, making it an effective model to study the pathogenesis of PD.

Abstract: Objective To investigate the inhibitory effect of miR-4539 on the growth of glioma cells. Methods The expression levels of miR-4539 in glioma samples and 7 glioma cell lines were detected by RT-PCR. CCK-8 method , flow cytometry and Western blot were used to detect the role of miR-4539 in glioma cells. Dual luciflucase assay was used to verify whether Foxp1 is a direct target of miR-4539. To investigate the inhibitory effect of miR-4539 transfection on tumor growth in mice, a mouse transplanted tumor model was constructed. Results (1) The expression level of miR-4539 in glioma tissues was significantly lower than that in normal brain tissues (P<0.05). The expression level of miR-4539 in 7 commonly used human glioma cell lines (U87, U251, U373, T98G, LN18, LN229, SF295) was significantly lower than that in human normal glioma cell line HEB (P<0. 05). (2) Compared with the miR-NC group, the expression levels of miR-4539 in T98G cells and LN18 cells were significantly increased 72 h after transfection of miR-4539 (P<0. 05). CCK-8 showed that the overexpression of exogenous miR-4539 significantly inhibited the proliferation of T98G and LN18 cells. Meanwhile, T98G and LN18 cell cycle arrest was induced, and the percentage of G0 / G1 phase cells was increased, while the percentage of S phase cells was decreased, and the expression levels of cell cycle regulatory proteins cyclinD1, cyclinE1 and Ser780 were also significantly decreased (P< 0.05). ( 3) Luciferase reports showed that Foxp1 is a direct target of miR-4539 and can be directly regulated by miR-4539. At 6 weeks after T98G cells were inoculated, the average volume and weight of transplanted tumor in the miR-4539-transfected mice were significantly smaller than those in the miR-NC group (P<0.05). (4) After overexpression of miR-4539 in T98G and LN18 cells, the expression of Foxp1 mrna and protein were significantly decreased. Immunofluorescence result also confirmed that miR-4539 reduced the expression of Foxp1 in T98G and LN18 cells. Conclusions MiR-4539 acts as a tumor suppressor by targeting Foxp1, which is expected to be a new target for the diagnosis and treatment of gliomas.

Abstract:Laboratory animals are important in teaching and scientific research, and qualified laboratory animals are an important prerequisite for scientific research. The establishment of scientific and standardized laboratory animal barrier facilities provides specific pathogen-free laboratory animals and platform support to carry out animal research. This article discusses the specific pathogen-free barrier facility for laboratory animals in the School of Pharmaceutical Sciences of Guangzhou University of Chinese Medicine as an example to introduce the operation mode of the laboratory animal barrier facility from the aspects of construction, management of regulations, personnel training and management, sterilization and cleaning, and waste disposal. We also propose relevant solutions to common problems encountered in the management process. Finally, some opinions on the future direction of laboratory animal barrier facilities will be put forward to provide significant information for the construction and management of laboratory animal barrier facility.

Abstract:Long noncoding RNAs ( lncRNAs) are a group of noncoding RNAs of more than 200 nucleotides in length. Accumulating research has unearthed increasing evidence that lncRNA wass are widely involved in the regulation of pathophysiological processes and affect the establishment and progression of human diseases including cancers. HAGLR opposite-strand lncRNA is highly expressed in many tumors, playing important roles in regulating tumors’ malignant behaviors. This paper reviews the expression and mechanisms of action of the HAGLR opposite-strand lncRNA in tumors.

Abstract:Rheumatoid arthritis ( RA) is a common autoimmune disease characterized by chronic synovial inflammation with joint cartilage and bone damage. Under Traditional Chinese Medicine, RA is categorized as a “ Bi disease.” Various RA models have been developed, including induced model, spontaneous genetic modification model, and model of Traditional Chinese Medicine syndrome. These models were reviewed and summarized in terms of their theoretical basis, typical characteristics, evaluation method , main usages, and degree of agreement. This paper also deals with the relationship between intestinal flora and RA to provide a reference for follow-up research.

Abstract:Air pollution affects not only sperm quality, such as the amount of sperm, sperm concentration, motility, progressive movement, morphology and other physical characteristics, but also the sperm genome, such as DNA fragmentation index and chromosome integrity. Air pollution has also been shown to influence male fertility by affecting the testosterone level or even testicular tissue cells. This review summarizes these issues on two levels: epidemiologically at the population level and from findings in animal research. This review also presents four possible mechanisms by which air pollutants affect spermatogenesis and development: as endocrine disruptors, by inducing reactive oxygen species, by destroying the blood-testosterone barrier, and by causing DNA mutations and epigenetic modifications. Finally, this review surveys recent studies suggesting medicines that have protective effects on sperm development.

Abstract:Vascular cognitive impairment (VCI) is a clinical syndrome in which at least one cognitive domain is damaged by cerebrovascular disease and vascular risk factors. The pathological manifestations include changes in vascular function, tissue damage, and nerve degeneration. Post-stroke cognitive impairment (PSCI) is a major subtype of VCI, which accounts for most VCI. Pathological mechanism research and drug development for PSCI have mostly relied on VCI animal models. As researchers have put forward and discussed in-depth the PSCI concept, we found that the pathological characteristics and main damaged cognitive areas of the two are not exactly the same. Therefore, it is necessary to establish an animal model with the clinical features of PSCI. There are many types of experimental animal models for VCI, and a PSCI research model should be distinguished from a VCI animal model. This article introduces the characteristics and impaired cognitive domains of VCI and PSCI, summarizes and preliminarily evaluates common VCI and PSCI experimental animal models from the perspective of model construction, and provides useful suggestions for VCI and PSCI research.

Abstract:Arrhythmia is an early abnormal manifestation of the heart. Atrial fibrillation is the most common arrhythmia in the clinic. However, its pathophysiological mechanism has not been fully elucidated. The risk of arrhythmias in drug therapy and the high cost of catheter ablation are clinical challenges. In recent years, metabonomics has made great progress in revealing the biomarkers and pharmacological effects of atrial fibrillation. This article reviews the pathogenesis, metabonomics research method , and biomarkers of atrial fibrillation to expand research ideas to prevent and treat atrial fibrillation.

Abstract:Ischemic cerebrovascular disease ( ICVD) is a common central nervous system disease with high morbidity and mortality. Cerebral collateral circulation has a positive compensatory effect on ICVD, which is often caused by atherosclerosis. In recent studies, various physiological and pathological processes of cerebrovascular atherosclerosis and establishment of collateral circulation were closely related to miRNA that has the potential to be used as a new biomarker for diagnosis and evaluation of ICVD. This article reviews the relationship between miRNA and cerebrovascular atherosclerosis, and the establishment of collateral circulation in ICVD.

Abstract:Acute myocardial infarction (AMI) can cause dramatic remodeling of the heart function and structure. These effects not only exist in the infarcted area, but also in the non-infarcted area. Myocardial dysfunction in the non- infarcted zone widely exists in patients with myocardial infarction, and the abnormal function of the non-infarcted area is an important predictor for the prognosis of AMI patients. Several related clinical and animal studies have also suggested that the regulation of non-infarcted areas is important to maintain cardiac function. Hence, studies on the manifestation, mechanism, and treatment of myocardial dysfunction in the non-infarcted area can provide valuable insights and guidance for myocardial function preservation in myocardial infarction patients. We reviewed the clinical and animal studies related to non-infarcted myocardium after acute myocardial infarction to provide ideas for the treatment and new intervention ideas of AMI .

Abstract:Programmed cell death (PCD) is a form of cell death regulated by genes. It plays an important role in the occurrence and development of tumors and other diseases. According to its occurrence, mechanism of action, and morphological characteristics, it can be divided into apoptosis, necroptosis, ferroptosis, pyroptosis and autophagy, among others. Long noncoding RNAs are noncoding RNAs of more than 200 nucleotides in length, which participate in the regulation of PCD by directly or indirectly affecting the expression of intracellular proteins and other molecules. This paper summarizes relevant literature on lncRNAs’ involvement in the regulation of PCD, which is expected to provide different pathways for further research on lncRNAs and PCD, as well as new ideas for diagnosis, treatment, and prevention of related clinical diseases.