1.Association between Arachidonic Acid Metabolism and Cervical Cancer
Xinrui PENG ; Zhen JIA ; Fengxian QI
Journal of Medical Research 2024;53(12):110-115
Objective To explore the association between arachidonic acid(AA)metabolism and cervical cancer(CC),to provide new ideas for metabolic therapies for CC.Methods The activity and migration ability of CC cells after AA intervention were detected by CCK-8 assay and cell scratch assay,respectively.Bioinformatics analysis was performed using GEPIA 2 and GSCA databases to study the correlation between key enzymes of AA metabolism(COX2,ALOX15)and the progression,prognosis,pathway activation,and tumor immunity of CC.The mRNA expression of inflammatory factors interleukin-6(IL-6),monocyte chemoattractant protein-1(MCP-1),tumor necrosis factor-α(TNF-α),interferon-γ(IFN-γ),cyclooxygenase 2(COX2),and arachidonic acid lipoxygenase 15(ALOX15)were detected by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR).Results A A at 5μmol/ml significantly promoted the growth of CC cells(t=7.672,P=0.0166)and increased the relative cell migration rate by 30%at the same concentration(t=6.672,P=0.0026).And the expression levels of inflammatory factors also showed significant differences(P<0.05).Further bioinformatics analysis revealed that the expression levels of key enzymes of AA metabolism,COX2 and ALOX15,were significantly up-regulated in CC(P<0.05),which also different in different stages and increased the risk of poor prognosis in patients.Among them,COX2 may accelerate the progression of CC by decreasing the level of tyrosine kinase metabolism and exacerbating DNA damage,and ALOX15 may form a tumor inflammatory environment by increasing the degree of infiltration of resting CD8+T cells and B lymphocytes.Conclusion AA metabolism promotes the proliferation and migration of CC cells and induces changes in the tumor inflam-matory microenvironment,in which its metabolic key enzymes,COX2 and ALOX15,may play an important role.
2.Association between Arachidonic Acid Metabolism and Cervical Cancer
Xinrui PENG ; Zhen JIA ; Fengxian QI
Journal of Medical Research 2024;53(12):110-115
Objective To explore the association between arachidonic acid(AA)metabolism and cervical cancer(CC),to provide new ideas for metabolic therapies for CC.Methods The activity and migration ability of CC cells after AA intervention were detected by CCK-8 assay and cell scratch assay,respectively.Bioinformatics analysis was performed using GEPIA 2 and GSCA databases to study the correlation between key enzymes of AA metabolism(COX2,ALOX15)and the progression,prognosis,pathway activation,and tumor immunity of CC.The mRNA expression of inflammatory factors interleukin-6(IL-6),monocyte chemoattractant protein-1(MCP-1),tumor necrosis factor-α(TNF-α),interferon-γ(IFN-γ),cyclooxygenase 2(COX2),and arachidonic acid lipoxygenase 15(ALOX15)were detected by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR).Results A A at 5μmol/ml significantly promoted the growth of CC cells(t=7.672,P=0.0166)and increased the relative cell migration rate by 30%at the same concentration(t=6.672,P=0.0026).And the expression levels of inflammatory factors also showed significant differences(P<0.05).Further bioinformatics analysis revealed that the expression levels of key enzymes of AA metabolism,COX2 and ALOX15,were significantly up-regulated in CC(P<0.05),which also different in different stages and increased the risk of poor prognosis in patients.Among them,COX2 may accelerate the progression of CC by decreasing the level of tyrosine kinase metabolism and exacerbating DNA damage,and ALOX15 may form a tumor inflammatory environment by increasing the degree of infiltration of resting CD8+T cells and B lymphocytes.Conclusion AA metabolism promotes the proliferation and migration of CC cells and induces changes in the tumor inflam-matory microenvironment,in which its metabolic key enzymes,COX2 and ALOX15,may play an important role.
3.Preliminary study of familial nonsyndromic tooth agenesis caused by ectodysplasin A mutation
WANG Huihui ; WU Qing ; XU Bin ; LING Qi ; WU Yiqun
Journal of Prevention and Treatment for Stomatological Diseases 2023;31(11):768-773
Objective:
To explore the pathogenic genes in a Chinese family affected by nonsyndromic tooth agenesis so as to study the pathogenesis of oligodontia.
Methods :
Hospital ethical approval and informed consent of the patients and family members were obtained. Clinical data of the proband and close family members were collected, peripheral venous blood was collected, and DNA was extracted. Gene sequencing was performed through whole-exome sequencing, and then the screened pathogenic genes were verified by Sanger sequencing. The three-dimensional structure of the mutant proteins was analyzed and compared with the wild-type using bioinformatics tools.
Results:
The two patients with congenital majority tooth loss in this family were cousins, and there were no other patients with congenital majority tooth loss in the family. Besides congenital multiple tooth loss, the two patients had no obvious hair abnormalities, finger/toe abnormalities, sweating abnormalities or other abnormal manifestations of ectodermal tissue. We found a mutant gene that in this family by carrying out gene sequencing of the patients and their close family members. A novel EDA (ectodysplasin A) missense mutation c.983C>T (p. Pro328Leu) was identified, which changed the encoded amino acid from proline (Pro) to leucine (Leu). Analysis of the mutation site showed that the site was highly conserved, and three-dimensional structure modeling also found that it changed the structure of EDA.
Conclusion
A novel EDA missense variant (c.983C>T, p.Pro328Leu) was first identified in a Chinese family with nonsyndromic tooth agenesis, extending the mutation spectrum of the EDA gene.
4.Potential Mechanism of Shenling Baizhusan in Disease Treatment: A Review
Jingjiang LAI ; Xiaoli ZHUO ; Fengxian JIANG ; Lei LIU ; Jingliang WANG ; Fanghua QI ; Guobin FU
Chinese Journal of Experimental Traditional Medical Formulae 2022;28(20):267-273
Shenling Baizhusan is a traditional Chinese medicine compound prescription formulated on the basis of Si Junzitang (Ginseng Radix et Rhizoma, Atractylodis Macrocephalae Rhizoma, Poria, Glycyrrhizae Radix et Rhizoma). It has excellent functions of replenishing Qi, invigorating spleen, draining dampness, and checking diarrhea, and is one of the classical prescriptions of ''reinforcing earth to generate metal''. This prescription is primarily used in clinical practice to treat malnutrition in children, chronic diarrhea, gastrointestinal dysfunction, and other disorders. In addition, it has a good effect on gastrointestinal adverse reactions associated with radiotherapy and chemotherapy. With the booming of molecular biology, researchers have revealed the role of Shenling Baizhusan in the treatment of diseases, especially the mechanism of regulating different signaling pathways. We retrieved 26 relevant papers (4 written in English and 22 in Chinese) published in recent 5 years from 6 databases including China National Knowledge Infrastructure (CNKI), Wanfang Data, VIP, PubMed, Cochrance Library, and Excerpta Medica Database (Embase). On the basis of these papers, we summarized the mechanisms of Shenling Baizhusan in disease treatment. In the animal model of inflammatory bowel disease, Shenling Baizhusan can protect gastrointestinal mucosa by regulating the activation of nuclear factor kappa-B (NF-κB), mitogen-activated protein kinase (MAPK), Janus kinase/signal transducer and activator of transcription (JAK/STAT), and myosin light chain kinase-myosin light chain (MLCK-MLC) signaling pathways. In the animal model of non-alcoholic fatty liver disease, Shenling Baizhusan regulates the activation of phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway and Kelch-like ECH-associating protein 1/NF-E2-related factor 2/advanced glycation end-products (KEAP1/NRF2/AREs) signaling pathway, thus alleviating the lipid metabolism disorder induced by high-fat diet and reducing liver lipid accumulation and inflammatory response. In the animal model of lung cancer with bone metastasis, Shenling Baizhusan regulates the activation of PI3K/Akt/mTOR signaling pathway, thus playing an analgesic role. By summarizing the mechanisms of Shenling Baizhusan in treatment of different disease models from signaling pathways, we aim to provide clues for the in-depth study of this prescription.
5.Investigation of leprosy survivors in Fengxian District, Shanghai
Qi SUN ; Qun LU ; Yao-zhong QIAN ; Peng LI ; Wei XU ; Lin ZHANG ; Bai-chen LI ; Xiu LI
Shanghai Journal of Preventive Medicine 2021;33(8):762-766
Objective:To understand the current living and health status of leprosy survivors in Fengxian District, Shanghai, and to provide scientific evidence for improving their quality of life. Methods:In January 2018-June 2020, professionally trained CDC staff performed a household investigation on 41 patients with leprosy (case group) and 82 non-leprosy persons (control group) every year. Living and health status, and routine laboratory examinations such as blood pressure, blood glucose, and blood lipids were monitored. Results:Majority of the patients with leprosy had low educational level (68.29% being primary school) and were mostly farmers (51.22%).The patients had abnormal residual Ⅱ level 5 (12.20%) and mostly were tb-like (TT) (53.66%). Moreover, some patients were not incapacitated (46.34%), had no family financial difficulties (29.27%), did not acquire the national subsistence allowance policy (58.54%), and asked for "regular physical examination" (68.29%).Compared to the 82 control persons, the patients with leprosy had significantly different body mass index (BMI) and blood pressure (
6.Histology research on repairing of rabbit articular cartilage defects with naringin and tissue engineering cartilage
Chungen LI ; Yi QU ; Chao YE ; Jing CHEN ; Fengxian WANG ; Pengyang LI ; Suhua LI ; Jingpei REN ; Jian QI
Chinese Journal of Tissue Engineering Research 2014;(20):3165-3171
BACKGROUND:At present, there are many methods to treat cartilage defects, but none radical y repairs the articular cartilage defects.
OBJECTIVE:To histological y verify the effect of naringin combined with tissue engineering cartilage on the repair of rabbit articular cartilage defects.
METHODS:Rabbit bone marrow mesenchymal stem cells fol owing in vitro proliferation were compounded onto acellular dermal matrix, which was then implanted into rabbit knee cartilage defects. Naringin was also given by lavage. Hematoxylin-eosin staining, Masson trichrome staining, toluidine blue dyeing, type II col agen staining and type X col agen staining were performed in the repaired tissue.
RESULTS AND CONCLUSION:After 8 weeks post-surgery, the defects repaired with the naringin and stem cells composite were turned into milky-white and transparent smooth tissue. The defective tissue which was repaired, was very similar to normal cartilage tissue, with smooth surface. After the histology research, we found that the defect tissue was fil ed with new cartilage tissue. Results indicated that naringin combined with tissue engineering cartilage can promote the repair of articular cartilage defects in rabbits.


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