الملخص
This study analyzed the characteristics and change trend of Guangzhou citizens' demands related to vaccination through government hotlines 12345 and 12320 from 2018 to 2020. It understood the hotspots and needs of the public for vaccination work, analyzed the problems existing in vaccination work, and provided reference and suggestions for health departments to improve vaccination services and formulate relevant policies: to timely improve the professional ability and knowledge reserve of hotline personnel; to strengthen the construction of vaccination service system;to optimize the appointment vaccination service application; to scientifically purchase HPV vaccine and ensure the production and supply of vaccine.
الموضوعات
Humans , Government , Hotlines , Papillomavirus Vaccines , Vaccinationالملخص
The present study optimized the extraction of flavonoids from Lonicera rupicola Hook. f. et Thoms(LRH) and explored its pharmacological effects, such as resisting inflammation, relieving pain, enhancing immunity, and inhibiting pyroptosis, aiming to provide data support and scientific basis for the development and utilization of LRH. Response surface methodology(RSM) was applied to optimize the extraction of flavonoids from LRH based on the results of single-factor experiments. Anti-inflammatory and analgesic effects of LRH flavonoids were evaluated via inflammation and pain models in mice, such as xylene-induced ear swelling, carrageenan-induced footpad swelling, writhing caused by acetic acid, and paw licking. The effect of LRH flavonoids on the carbon clearance index of monocytes and serum immunoglobulin A(IgA) and IgM levels was analyzed on the immunosuppression model induced by cyclophosphamide in mice. The anti-oxidative effect in vivo of LRH flavonoids on liver superoxide dismutase(SOD), catalase(CAT), and malondialdehyde(MDA) levels was determined based on the chronic/subacute aging model in mice induced by D-galactose. The levels of cysteinyl aspartate specific proteinase-1(caspase-1), interleukin-1β(IL-1β), and IL-18 in the supernatant of J774 A.1 mononuclear phagocytes were detected to evaluate the effect of LRH flavonoids on the pyroptosis of mononuclear phagocytes in mice induced by the combination of lipopolysaccharide(LPS) and adenosine triphosphate(ATP). Meanwhile, the effect of LRH flavonoids on the cAMP-PKA signaling pathway was also explored. The optimum conditions for the extraction of LRH flavonoids are listed below: extraction temperature of 65 ℃, the ethanol concentration of 50%, extraction time of 60 min, a material-liquid ratio at 1∶25, and the yield of LRH flavonoids of 0.553%. RSM determined the multiple quadratic regression equation model of response value and variables as follows: the yield of LRH flavonoids=0.61-0.48A+0.1B+0.029C-0.014D+0.32AB+0.04AC-0.012AD-0.02BC+0.037BD-0.031CD-0.058A~2-0.068B~2-0.069C~2-0.057D~2. LRH flavonoids could effectively inhibit ear swelling and footpad swelling, reduced acetic acid-induced writhing, and delayed the paw licking response time in mice. Additionally, LRH flavonoids could improve the carbon clearance index in immunosuppressed mice, potentiate the activities of SOD and CAT and reduce MDA levels in the liver of aging mice induced by D-galactose, and effectively inhibit macrophage pyroptosis by decreasing the levels of caspase-1, IL-1β, and IL-18. The results reveal that LRH flavonoids possess excellent pharmacological activities such as resisting inflammation and oxidation, relieving pain, and enhancing immunity. They can inhibit pyroptosis by enhancing the cAMP-PKA signaling pathway. The results of this study can underpin the pharmacological research, development, and utilization of LRH.
الموضوعات
Animals , Mice , Analgesics/therapeutic use , Edema/drug therapy , Flavonoids/therapeutic use , Inflammation/drug therapy , Lonicera , Mice, Inbred ICR , Pain/drug therapy , Plant Extracts/therapeutic use , Pyroptosisالملخص
BACKGROUND@#Acute lung injury (ALI) is characterized by an acute inflammatory process, and oxidative stress in the lung tissue leads to a lack of effective therapeutics. This study aimed to identify whether the overexpression of transcription factor EB (TFEB) regulates mitophagy to protect against lipopolysaccharide (LPS)-induced ALI.@*METHODS@#We detected the expression of inflammatory factors, cytochrome c (Cyt.c) and nicotinamide adenine dinucleotide phosphate (NADPH), and autophagy-related proteins and observed the changes in lung histopathology induced by ALI in rats and the changes in the cell ultrastructure of primary alveolar type II epithelial cells induced by changing the expression of TFEB in the context of ALI.@*RESULTS@#The overexpression of TFEB could reduce the expression of proinflammatory factors, such as IL-1 and IL-6, and increase the expression of anti-inflammatory factors, such as IL-10, both in vitro and in vivo. In addition, the overexpression of TFEB could reduce the Cyt.c and NADPH levels both in vivo and in vitro. The overexpression of TFEB could upregulate the expression of autophagy-related proteins, such as lysosomal-associated membrane protein 1 (LAMP1), microtubule-associated protein light chain 3B (LC3B), and Beclin both in vivo and in vitro, and promote mitochondrial autophagy. The overexpression of TFEB significantly improved the histopathologic changes induced by LPS-induced ALI in rats. However, low TFEB expression produced the opposite results.@*CONCLUSION@#TFEB overexpression can decrease inflammation and mitochondrial damage in the lung tissue and alveolar epithelial cells through regulating mitochondrial autophagy to protect against LPS-induced ALI. Therefore, TFEB is likely a potential therapeutic target in LPS-induced ALI.
الملخص
Background@#Acute lung injury (ALI) is characterized by an acute inflammatory process, and oxidative stress in the lung tissue leads to a lack of effective therapeutics. This study aimed to identify whether the overexpression of transcription factor EB (TFEB) regulates mitophagy to protect against lipopolysaccharide (LPS)-induced ALI.@*Methods@#We detected the expression of inflammatory factors, cytochrome c (Cyt.c) and nicotinamide adenine dinucleotide phosphate (NADPH), and autophagy-related proteins and observed the changes in lung histopathology induced by ALI in rats and the changes in the cell ultrastructure of primary alveolar type II epithelial cells induced by changing the expression of TFEB in the context of ALI.@*Results@#The overexpression of TFEB could reduce the expression of proinflammatory factors, such as IL-1 and IL-6, and increase the expression of anti-inflammatory factors, such as IL-10, both in vitro and in vivo. In addition, the overexpression of TFEB could reduce the Cyt.c and NADPH levels both in vivo and in vitro. The overexpression of TFEB could upregulate the expression of autophagy-related proteins, such as lysosomal-associated membrane protein 1 (LAMP1), microtubule-associated protein light chain 3B (LC3B), and Beclin both in vivo and in vitro, and promote mitochondrial autophagy. The overexpression of TFEB significantly improved the histopathologic changes induced by LPS-induced ALI in rats. However, low TFEB expression produced the opposite results.@*Conclusion@#TFEB overexpression can decrease inflammation and mitochondrial damage in the lung tissue and alveolar epithelial cells through regulating mitochondrial autophagy to protect against LPS-induced ALI. Therefore, TFEB is likely a potential therapeutic target in LPS-induced ALI.
الملخص
With the emergence of the modified forms of acupuncture-moxibustion such as dry needle,the discipline acupuncture-moxibustion faces significant opportunities and challenges.The concept and treatment of acupuncture-moxibustion need to combine with modern medicine to consolidate the effectiveness and apply the research results to guide clinical treatment.By reviewing the brief history of acupuncture-moxibustion in the Western countries and summarizing the definitions,this article was to propose the trend and development strategies of this discipline in the future.
الملخص
Objective:To investigate the relationship between LncRNA MALAT-1 and miR-205 in non-small cell lung cancer and the mechanism of biological behavior in lung cancer cells.Methods: The expression of LncRNA MALAT-1 in different non-small cell lung cancer was detected by qPCR.The interaction between MALAT-1 and miR-205 was detected by double luciferase reporter gene.Transwell invasion assay and scratch test were used to detect the changes of invasion and migration abilities of lung cancer cells after silencing MALAT-1 and the recovery the abilities after inhibition of miR-205 expression.The tumor volume and quality of lung cancer cells were detected by subcutaneous tumor formation in nude mice after silencing MALAT-1.Results:Compared with other lung cancer cell lines,the expression of MALAT-1 was the highest and the expression level of miR-205 was the lowest in A549 cells.The double luciferase assay confirmed that MALAT-1 could specifically bind to 3′UTR of miR-205,and could regulate the expression and activity of miR-205.Inhibition of MALAT-1 expression could reduce the migration and invasion of lung cancer cells;while inhibiting the expression of miR-205 level,the migration and invasion of lung cancer cells could recovery.The tumor volume and quality of lung cancer cells were reduced after silencing MALAT-1 in subcutaneous tumorigenesis of nude mice.Conclusion: MALAT-1 can regulate the expression of miR-205 and affect the invasion and migration of lung cancer cell line A549.
الملخص
Objective:To investigate the effect of miR-210 on the migration and proliferation of lung cancer cells. Methods:The expression of miR-210 in normal lung tissues and lung cancer tissues were detected by qPCR. The expression of Mex3B in lung cancer tissues and adjacent tissues were detected by qPCR. qPCR was used to detect the expression of miR-210 in different lung cancer cell lines(A549,H1299,H1650 and H358). The effect of miR-210 on the transcription of Mex3B was detected by double luciferase reporter gene system. The effect of miR-210 expression on the activity of lung cancer cells was detected by cell viability assay. The effect of miR-210 on the proliferation of A549 cells were detected by plate cloning assay. Transwell invasion assay were used to detect the effect of miR-210 on the invasion ability of lung cancer cell line A549. Results:Compared with adjacent tissues,the expression of miR-210 were significantly decreased in lung cancer tissues,Mex3B were lower in lung cancer. Double luciferase reporter gene system results showed that miR-210 can directly regulate the transcriptional activity of Mex3B. The invasion and proliferation ability of lung cancer cell line were significantly reduced after inhibition of miR-210. Conclusion:miR-210 can target regulate the expression of Mex3B, and affects the invasion and proliferation of lung cancer cells.
الملخص
Objective:To investigate the effect of miR-210 on the migration and proliferation of lung cancer cells. Methods:The expression of miR-210 in normal lung tissues and lung cancer tissues were detected by qPCR. The expression of Mex3B in lung cancer tissues and adjacent tissues were detected by qPCR. qPCR was used to detect the expression of miR-210 in different lung cancer cell lines(A549,H1299,H1650 and H358). The effect of miR-210 on the transcription of Mex3B was detected by double luciferase reporter gene system. The effect of miR-210 expression on the activity of lung cancer cells was detected by cell viability assay. The effect of miR-210 on the proliferation of A549 cells were detected by plate cloning assay. Transwell invasion assay were used to detect the effect of miR-210 on the invasion ability of lung cancer cell line A549. Results:Compared with adjacent tissues,the expression of miR-210 were significantly decreased in lung cancer tissues,Mex3B were lower in lung cancer. Double luciferase reporter gene system results showed that miR-210 can directly regulate the transcriptional activity of Mex3B. The invasion and proliferation ability of lung cancer cell line were significantly reduced after inhibition of miR-210. Conclusion:miR-210 can target regulate the expression of Mex3B, and affects the invasion and proliferation of lung cancer cells.