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26 December 2020, Volume 10 Issue 6 Previous Issue    Next Issue

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Study on the Mechanism of Radix Paeoniae Rubra on Hepatocellular Carcinoma Based on Network Pharmacology YOU Si-han, BAI Jing-ru, WANG Zhi-bao, TAN Xiao-hong, GUO Chun-yan 2020, 10 (6):  1-12.  DOI: 10.3969/j.issn.2095-1396.2020.06.001 Abstract ( 273 )   PDF (11223KB) ( 42 )   Objective:To predict the mechanism of Radix Paeoniae Rubra in the treatment of hepatocellular carcinoma(HCC)by network pharmacology. Methods:Through TCMSP database(https://tcmspw.com/tcmspsearch.php)，the chemical constituents of Radix Paeoniae Rubra were searched，and the targets of Radix Paeoniae Rubra were predicted by STD database and SEA database. Through OMIM database(http://www.omim.org)，drugbank database(https:// www.drugbank.ca/)and TTD database(http://db.idrblab.net/ttd/)，the corresponding targets of HCC were collected. Then, the common targets from both active ingredient targets and HCC disease targets were obtained. The String platform was used to collect liver cancer disease-related target proteins, and GO analysis was performed with David database. Protein-protein interaction (PPI) network was constructed by Cytoscape 3.2.1 software, and the core targets were obtained by topological analysis. The mechanism of Radix Paeoniae Rubra on HCC was further analyzed.  Results:A total of 28 compounds and 442 targets from Radix Paeoniae Rubra were obtained from TCMSP database. A total of 148 HCC-related disease targets were retrieved from OMIM, DrugBank and TTD databases. Twenty-three common targets from both active ingredient targets and HCC disease targets were obtained. There were 193 nodes and 722 edges in the protein- protein interaction network，and 95 nodes，439 edges and 21 core targets were obtained by topological index screening. A total of 561 biological processes，85 cellular components and 130 molecular functions were obtained by GO annotation. Conclusion:Network pharmacology intuitively shows that Radix Paeoniae Rubra has multiple components，multiple targets and multiple pathways in the treatment of HCC. This study provides a theoretical basis for the follow-up development of medicines for the treatment of HCC. Related Articles | Metrics

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Effects of Atorvastatin Calcium on Nerve Function in Rats with Non-Cardiac Ischemic Stroke WENG Ying-hua 2020, 10 (6):  13-17.  DOI: 10.3969/j.issn.2095-1396.2020.06.002 Abstract ( 59 )   PDF (3845KB) ( 9 )   Objective:To study the effect of atorvastatin calcium on the neurological function of rats with non-cardiac ischemic stroke and its mechanism. Methods:Thirty SD rats were randomly divided into sham operation group，model group and atorvastatin group，with 10 in each group. Non-cardiac ischemic stroke models were established for rats in the model group and the atorvastatin group. The rats in the atorvastatin group were given continuous intragastric administration of atorvastatin(1 mg·kg-1·d-1)for 2 w. For the sham operation group, the internal carotid artery was not blocked，and the sham operation group and the model group were given continuous intragastric administration of an equal volume of 0.9% sodium chloride solution. Observe the differences in various indicators such as neural function assessment，brain tissue pathological changes，neuronal apoptosis，and serum inflammatory factor levels(IL-6，TNF-α and IL-1β)among the groups，and Western blotting method to observe each group different expressions of rat neuronal apoptosis-related protein TLR4，nuclear transcription factor NF-κB p65，pIκB，Cleaved Caspase-3. Results:The neurological deficit score，HE staining pathological section observation，apoptosis rate，serum IL-6，TNF-α and IL-1β in the atorvastatin group were significantly improved compared with the model group(P<0.05). Western blotting showed that TLR4，NF-κB p65，p-I κB，and Cleaved Caspase-3 in the atorvastatin group were significantly down-regulated compared with the model group(P<0.05). Conclusion: Atorvastatin calcium inhibits T L R 4 a n d n u c l e a r t r a n s c r i p t i o n f a c t o r N F - κ B p 6 5 ，i n h i b i t s n e u r o n a l a p o p t o s i s i n r a t s w i t h n o n - c a r d i a c ischemic stroke and improves neurological dysfunction through this pathway. Related Articles | Metrics

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The Effect and Mechanism of Aspirin on Neuronal Cell Apoptosis in Ischemic Cerebral Infarction WU Jian, HUANG Yu-mei, ZHANG Ling-ling, LV Xiu-hua 2020, 10 (6):  18-22.  DOI: 10.3969/j.issn.2095-1396.2020.06.003 Abstract ( 80 )   PDF (2175KB) ( 21 )   Objective:To explore the effect of aspirin on neuronal apoptosis and its mechanism in rats with ischemic cerebral infarction. Methods:90 healthy SD rats were randomly divided into 3 groups，named the control group，the model group，and the aspirin group(50 mg·kg-1)，each group with 30 cases. Except for the control group，the other two groups were treated with common carotid artery obstruction. To establish a rat model of ischemic cerebral infarction. The aspirin group was given continuous intragastric administration of aspirin at a dose of 50 mg·kg-1 5 days before modeling. On the 6th day，3 groups of rats were sacrificed. The TdT-mediated dUTP Nick-End Labeling (TUNEL) method was used to detect neuronal cell apoptosis in rat brain tissue. Western blot technology was used to detect rat brain tissue nerve. The expression of B-cell lymphoma-2 (Bcl-2)and Bcl2-associated X(Bax)protein in metabolites and the release of Cyt-C. Results: The TUNEL method showed that the apoptosis rate of neuronal cells in the brain tissue of the aspirin group was significantly lower than that of the model group. The results of Western blot technology showed that the expression of Bcl-2 protein in the brain tissue of the aspirin group was significantly higher than that of the model group. The Bax protein expression and cytochrome C(Cyt-C)release amount were significantly lower than the model group，and the above differences were statistically significant(P<0.05). Conclusion:Aspirin can effectively reduce the neuronal cell apoptosis in brain tissue caused by ischemic cerebral infarction and play a neuroprotective effect. The mechanism may be related to reducing the release of mitochondrial Cyt-C，while increasing the expression of Bcl-2 protein and reducing Bax. The amount of protein expression is related. Related Articles | Metrics

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Optimization of the Extraction Process of Flavonoids from Fructus Aurantii by Response Surface Method LIU Xiao-hui, WANG Yin-yue, WANG Shi-ting, ZHENG Xiao-qing, TIAN Jia-ming, WANG Jin, ZHAO Yong-ming, 2020, 10 (6):  23-26.  DOI: 10.3969/j.issn.2095-1396.2020.06.004 Abstract ( 88 )   PDF (2913KB) ( 10 )   Objective:Box-Behnken experimental design was used to optimize the ultrasonic-assisted extraction process of the total flavonoids from Fructus Aurantii. Methods:Taking the extraction yield of total flavonoids from Fructus Aurantii as indexes，the single factor experiment and Box-Behnken experiment design were used to optimize the ethanol concentration，extraction time and material-to-liquid ratio. Results:The optimal condition established in this experiment was ethanol concentration of 14%，ultrasonic extraction time of 27 min， and material-to-liquid ratio of 1∶44. Under these optimal conditions，the extraction yield of the total flavonoids of Fructus Aurantii was 18.81 mg·g-1，which was in line with the predicted value of the model. Conclusion: Ultrasound-assisted extraction of total flavonoids from Fructus Aurantii is feasible with less time and higher extraction yield. This study provide the foundation for further research on Fructus Aurantii. Related Articles | Metrics

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Research Progress in Mechanism of Drug Resistance of Carbapenem-Resistant Klebsiella Pneumoniae ZHAN Xu-li, TANG Jian-hua 2020, 10 (6):  27-33.  DOI: 10.3969/j.issn.2095-1396.2020.06.005 Abstract ( 174 )   PDF (1111KB) ( 30 )   Carbapenem-resistant Klebsiella pneumoniae(Carbapenem-resistant Klebsiella pneumoniae，CRKP)is one of the important pathogenic bacteria isolated clinically and nosocomial infections. As the beta lactam class and aminoglycoside the wide use of broad-spectrum antibiotics， bacteria easy generation ultra broad spectrum beta lactamase，cephalosporins，enzyme and aminoglycoside modifying enzyme，to commonly used medicines including third-generation cephalosporin and aminoglycoside presents severe multiple drug resistance. Because CRKP is resistant to most antibiotics，it has become a very difficult problem in clinical treatment. It has become important to strengthen the monitoring of bacterial resistance and reduce bacterial resistance caused by overuse of antibiotics. Therefore，it is necessary to systematically sort out CRKP and discuss its drug resistance mechanism，so as to provide reference basis for rational selection of antibacterial drugs and optimization of medical resources in the future. Related Articles | Metrics

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Advances in Pharmacological Effects of Chrysophanol YUAN Xin-ru, ZHANG Dan-shen 2020, 10 (6):  34-40.  DOI: 10.3969/j.issn.2095-1396.2020.06.006 Abstract ( 262 )   PDF (1111KB) ( 58 )   Chrysophanol is one of the effective monomers of anthraquinones that extracted from traditional Chinese medicine. It exists in the form of free aglycon in rhubarb， fleeceflower root，polygonum cuspidatum，cassia，pinellia，etc. Studies have found that chrysophanol has good pharmacological activities in neuroprotection，anti-oxidation，anti-cancer， anti-inflammatory，antibacterial and anti-virus，and promotion of fat metabolism. Although there are many studies on the pharmacological activity of chrysophanol，the overall review of it is relatively few. This article provides a comprehensive review of the pharmacological effects of chrysophanol，and provides valuable references for further research and clinical applications. Related Articles | Metrics

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Research Progress of SIRT1 in Cerebral Ischemia-Reperfusion Injury ZHANG Jia-xiu, ZOU Yu-an 2020, 10 (6):  41-44.  DOI: 10.3969/j.issn.2095-1396.2020.06.007 Abstract ( 206 )   PDF (1019KB) ( 38 )   Acute ischemic stroke is a kind of disease with complicated pathogenesis and no effective treatment at present. Silencing information regulator 1(SIRT1)is a nicotinamide adenine dinucleotide(NAD+)-dependent deacetylase，and is one of the important regulators of aging，apoptosis and other physiological activities. Studies have shown that SIRT1 is closely related to the neuroprotective effect of cerebral ischemia-reperfusion injury and may be a new target for the treatment of acute ischemic stroke. Related Articles | Metrics

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Research Progress On The Relationship Between VASH-2 And Tumor XU Kai-lun, ZHANG Zhi-hua, GAO Yan-song 2020, 10 (6):  45-47.  DOI: 10.3969/j.issn.2095-1396.2020.06.008 Abstract ( 188 )   PDF (1033KB) ( 29 )   Angiogenesis is involved in the occurrence, invasion and metastasis of tumors, and plays an important role in the development of tumors. The Vasohibin family is a recently discovered regulatory factor that affects angiogenesis. VASH-1 and VASH-2 are important members of this family and are involved in tumor generation and development. VASH-1 plays a negative regulatory role in tumor pathogenesis, and VASH-2 promotes angiogenesis. This paper reviews the relationship between VASH-2 and tumors, discusses the role of VASH-2 in tumors, and provides new ideas for the development of blood vessel-targeted anti-cancer drugs. Related Articles | Metrics

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Relationship between Adult Hippocampus Neurogenesis and Alzheimer’s Disease DING Sheng-kai, LIU Qing-qing, LIU Xin-yang, SHANG Ya-zhen 2020, 10 (6):  48-53.  DOI: 10.3969/j.issn.2095-1396.2020.06.009 Abstract ( 377 )   PDF (1082KB) ( 86 )   Alzheimer’s disease(AD)is a common neurodegenerative disease in old age and has been published by world health organization(WHO)as one of the largest global public health issues facing mankind. The main clinical symptom is the progressive decline of learning and memory ability. The neuropathological changes of AD include senile plaque(SP)formed by β-amyloid protein(Aβ)of accumulated outside of neuon，neurofibrillary tangle(NFT) formed by hyperphosphorylated Tau protein of inside the neuron，neuron loss and degeneration， synapse decrease and so on. Especially，the abnormal neurogenesis is also involved in the neuropathological process of AD. There are many studies have showed that neurogenesis is a process of neural stem cells in hippocampal dentate gyrus of adult mammals to produce new neuron. The increased adult neurogenesis can compensate the injured neurons and save the learning and memory impairment. Then，the promotion of adult hippocampal neurogenesis may  be beneficial to treatment of AD. The present paper summarizes the relationship between the adult hippocampal neurogenesis and Alzheimer’s disease. Related Articles | Metrics

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Research Progress of High-Fat Diet and Alzheimer’s Disease HUANG Ying, HUO Yan-li, MING Yue, HAO Jun-rong 2020, 10 (6):  54-59.  DOI: 10.3969/j.issn.2095-1396.2020.06.010 Abstract ( 238 )   PDF (1104KB) ( 71 )   High-fat diet plays an important role in the pathogenesis of AD. This paper reviews the possible pathogenesis of Alzheimer’s disease in recent years，and further expounds the possible mechanism of high fat diet causing Alzheimer’s disease:High fat diet increases the content of saturated free fatty acids in plasma and speeds up the pathological process of AD; High fat diet promotes the occurrence of AD by influencing blood lipid levels;A high-fat diet will lead to the production of large amounts of fat and cause chronic inflammation，the inflammatory factors produced cross the blood-brain barrier and stimulate neuroinflammatory cells;High-fat food will affect the gut bacteria，which in turn affect the microbiota - brain - gut axis，then lead to the AD. Based on the above mechanisms，we can treat or prevent AD by reducing free saturated fatty acids， regulating lipid metabolism disorders，improving inflammation，and regulating intestinal flora. Related Articles | Metrics

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Research Progress on Related Mechanisms of Cerebral Ischemia-Reperfusion Injury LI Zhao-zhen, ZHANG Dan-shen 2020, 10 (6):  60-63.  DOI: 10.3969/j.issn.2095-1396.2020.06.011 Abstract ( 482 )   PDF (1018KB) ( 194 )   Cerebral ischemia-reperfusion injury can affect the outcome of the patient’s disease，even life-threatening. At present，the pathogenesis of cerebral ischemia-reperfusion injury includes inflammatory response，excitatory amino acid toxicity，intracellular calcium overload，free radical damage，energy metabolism disorder and cell apoptosis，etc. Many mechanisms influence each other and are complicated. This article summarizes the research on several main mechanisms of cerebral ischemia-reperfusion injury in recent years，and provides a basis for exploring and improving the research of cerebral ischemia-reperfusion injury. Related Articles | Metrics