1.Discussion on the Medical Humanities Education in the Perspective of Social Practice
Chinese Medical Ethics 2016;29(4):711-713
Lack of domestic medical humanistic education in medical schools leads to the low humanistic quali-ty of medical students, but humanistic quality of medical personnel is essential to medical activities. Taking into ac-count the actual domestic medical schools, for medical students, humanistic quality education in social practice should be the only way, which encompasses guiding medical students to pay attention to people′s livelihood, build-ing a social practice brand combined medicine and humanities, and implementing dynamic observation of humanis-tic education.
3.Discussion on the Cultural Integration in the Construction of Regional Medical Consortium
Shimei JIANG ; Xiu ZHONG ; Sheng ZHONG
Chinese Medical Ethics 2016;29(2):327-329
This paper stated the main contents of hospital cultural integration beginning of the necessary of it. Hospital cultural integration contained concept of symbiosis, management upgrade, strategic reorganization, recon-struction of responsibilities and rights, code of conduct, etiquette unity. The authors pointed out the current prob-lems of cultural integration:ideological understanding was lacking combined with the preference to technology over humanities;the integration mechanism was not perfect and the adaptation was terrible;integration planning was not systematic combined with the lack of investigation and research. The paper also put forward concrete paths to a-chieve the cultural integration in the process of construction of regional medical association:develop deep practical cultural integration programs;make policy to stabilize human resources;strengthen exchange of middle-level ca-dre posts;create an atmosphere that all persons participate in cultural integration.
4.Optimization of the Microwave-assisted Extraction of Total Organic Acids from Isatis indigotica by Or-thogonal Test
Liming LEI ; Yunkai JIANG ; Qian GAO ; Shimei LIU
China Pharmacy 2005;0(24):-
OBJECTIVE: To optimize the microwave-assisted extraction of total organic acids from Isatis indigotica. METHODS: With the dissolution rate of total organic acids as indexes, the content of total organic acids was determiend by acid-base titration and the three main factors including volume of solvent, microwave power and extraction time in the extraction process were optimized by orthogonal test. RESULTS: The optimal extraction process is to add 15 times amount of water and extract at a microwave power of 522 W for 20 minutes. Under the above condition, the extraction rate was 4.83%, close to the extraction yield achieved by water decoction for 2 h. CONCLUSION: The microwave-assisted extraction of total organic acids from Radix Isatidis is characterized by rapid, simple, efficient and energy-saving etc, thus deserving to be be popularized.
5.Chrysin promotes SMMC-7721 cell apoptosis by regulating MAPKs signaling pathway.
Xiaotong WEI ; Wenrui PENG ; Qi JIANG ; Qiang LI ; Zunyong FENG ; Zhilin QI ; Shimei QI
Journal of Southern Medical University 2018;38(10):1187-1194
OBJECTIVETo study the effect of chrysin in inducing apoptosis of human hepatic carcinoma cells and explore the possible mechanism.
METHODSHuman hepatic carcinoma SMMC-7721 cells treated with DMSO or chrysin at different concentrations (5-200 μg/mL) were examined for changes in the cell proliferation using CCK-8 assay. The morphological changes of SMMC-7721 cells were observed in response to treatment with 5, 10, or 20 μg/mL chrysin, and the changes in the cell nuclei were observed using DAPI nuclear staining. Annexin Ⅴ-FITC/PI flow cytometry was used to determine the cell apoptosis rate. The changes in the apoptosis-related proteins (PARP and caspase-3) and MAPKs signal pathway were detected with Western blotting.
RESULTSChrysin treatment obviously suppressed the proliferation of SMMC-7721 cells in a dose-dependent manner below the concentration of 60 μg/mL. Chrysin (20 μg/mL) also caused significantly increased cell apoptosis and significant cleavage of PARP and caspase-3. Chrysin significantly activated MAPKs signaling pathway in a time-and dose-dependent manner, with the peak activation level occurring at 15 min. Pretreatment of the cells with specific inhibitors of the MAPKs pathway obviously inhibited the effect of chrysin in inducing cell apoptosis.
CONCLUSIONSChrysin inhibits the proliferation and promotes apoptosis of SMMC-7721 cells by regulating the activation of MAPKs signaling.
6.Aloin induces apoptosis regulating the activation of MAPKs signaling pathway in human gastric cancer cells .
Ziqian WANG ; Hong TAO ; Yunfei MA ; Tuo TANG ; Qing ZHANG ; Qi JIANG ; Shimei QI ; Jiaping LI ; Zhilin QI
Journal of Southern Medical University 2018;38(9):1025-1031
OBJECTIVETo investigate the effect of aloin on apoptosis of human gastric cancer cells and explore the molecular mechanism.
METHODSGastric cancer MKN-28 and HGC-27 cells were cultured routinely in 1640 medium supplemented with 10% fetal bovine serum and 10% non-essential amino acids (for HGC-27 cells) and treated with different concentrations of aloin for different durations. The cell viability, cell nuclear morphology, and apoptotic rate of the cells were detected using CCK-8 assay, DAPI staining and AnnexinV-FITC/PI, respectively; Western blotting was used to detect the expression levels of PARP, procaspase 3 and the phosphorylation of p38, ERK and JNK. The cells were treated with specific inhibitors of p38, ERK and JNK, and the inhibitory effects on these pathways were detected with Western blotting; DAPI staining was used to detect the effects of inhibitors on apoptosis of gastric cancer cells.
RESULTSAloin dose-dependently inhibited the viability and induced apoptosis of HGC-27 and MKN-28 cells. Alion treatment obvious enhanced the phosphorylation of p38 and JNK but decreased ERK phosphorylation in the cells. Blocking ERK activation with the ERK inhibitor obviously enhanced aloin-induced cell apoptosis, where inhibiting p38 and JNK activation partly reversed alion-induced apoptosis in the cells.
CONCLUSIONSAloin induces apoptosis of human gastric cancer cells by activating p38 and JNK signaling pathways and inhibiting ERK signaling pathway.
7.Isoliquiritigenin induces HMOX1 and GPX4-mediated ferroptosis in gallbladder cancer cells.
Zeyu WANG ; Weijian LI ; Xue WANG ; Qin ZHU ; Liguo LIU ; Shimei QIU ; Lu ZOU ; Ke LIU ; Guoqiang LI ; Huijie MIAO ; Yang YANG ; Chengkai JIANG ; Yong LIU ; Rong SHAO ; Xu'an WANG ; Yingbin LIU
Chinese Medical Journal 2023;136(18):2210-2220
BACKGROUND:
Gallbladder cancer (GBC) is the most common malignant tumor of biliary tract. Isoliquiritigenin (ISL) is a natural compound with chalcone structure extracted from the roots of licorice and other plants. Relevant studies have shown that ISL has a strong anti-tumor ability in various types of tumors. However, the research of ISL against GBC has not been reported, which needs to be further investigated.
METHODS:
The effects of ISL against GBC cells in vitro and in vivo were characterized by cytotoxicity test, RNA-sequencing, quantitative real-time polymerase chain reaction, reactive oxygen species (ROS) detection, lipid peroxidation detection, ferrous ion detection, glutathione disulphide/glutathione (GSSG/GSH) detection, lentivirus transfection, nude mice tumorigenesis experiment and immunohistochemistry.
RESULTS:
ISL significantly inhibited the proliferation of GBC cells in vitro . The results of transcriptome sequencing and bioinformatics analysis showed that ferroptosis was the main pathway of ISL inhibiting the proliferation of GBC, and HMOX1 and GPX4 were the key molecules of ISL-induced ferroptosis. Knockdown of HMOX1 or overexpression of GPX4 can reduce the sensitivity of GBC cells to ISL-induced ferroptosis and significantly restore the viability of GBC cells. Moreover, ISL significantly reversed the iron content, ROS level, lipid peroxidation level and GSSG/GSH ratio of GBC cells. Finally, ISL significantly inhibited the growth of GBC in vivo and regulated the ferroptosis of GBC by mediating HMOX1 and GPX4 .
CONCLUSION
ISL induced ferroptosis in GBC mainly by activating p62-Keap1-Nrf2-HMOX1 signaling pathway and down-regulating GPX4 in vitro and in vivo . This evidence may provide a new direction for the treatment of GBC.
Animals
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Mice
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Carcinoma in Situ
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Chalcones/pharmacology*
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Ferroptosis
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Gallbladder Neoplasms/genetics*
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Glutathione Disulfide
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Kelch-Like ECH-Associated Protein 1
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Mice, Nude
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NF-E2-Related Factor 2/genetics*
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Reactive Oxygen Species
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Humans