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30 November 2023, Volume 20 Issue 6
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Mechanism of Anti-EBV Latent Membrane Protein-1 Monoclonal Antibodies in Promoting Apoptosis of HIV-associated EBV-positive Burkitt Lymphoma #br#
TU Xiaoyu, CHEN Yu, XIONG Yuhong, DENG Aihua, SUN Chunzhi, LIU Yang
2023, 20(6):  467-472.  doi:10.3870/j.issn.1672-8009.2023.06.001
Abstract ( 95 )   PDF (1986KB) ( 182 )  
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Objective To prepare and screen out the anti-EBV ( Epstein-Barr virus) latent membrane protein-1 monoclonal antibodies against Burkitt’s lymphoma (BL). Methods EBV latent membrane protein-1 ( LMP1) transmembrane domain 5 ( TMD5) was synthesized, and was used as the antigen to prepare the anti-TMD5 monoclonal antibodies by hybridoma method. ELISA assay was used to determine the titer of antibodies in mouse ascites. 7-AAD / Annexin V-PE in combination of flow cytometry (FCM) and JC-1 staining in combination of FCM were used to evaluate the apoptotic activity of BL cell line Daudi cells after treatment of monoclonal antibodies. Western blotting assay was used to determine the expression levels of p38-MAPK, IKK, NF-κB. Results After2 rounds of screening, monoclonal antibodies (R2-2-5E-6C and R2-2-8D-3A) were obtained. Both of those could specifically bind to TMD5 peptide, but had no immune response to GAPDH. Compared with these in the NC group, the percentage of Annexin V + 7-AAD + cells after treatment in the R2-2-5E-6C and R2-2-8D-3A groups were increased, the percentage of cells with JC-1fluorescence intensity less than 104 were increased, and the expression levels of intracellular p38-MAPK, IKK and NF-κB were decreased in the Daudi cells (P < 0. 05). Conclusion The obtainedanti-TMD5 monoclonal antibodies R2-2-5E-6C and R2-2-8D-3A could promote BL apoptosis throughthe inhibition of p38-MAPK / IKK / NF-κB pro-survival signaling pathway mediated by LMP1.
Protective Effect of Oxysophocarpine on Myocardial Ischemia-reperfusion Injury in Rats and Its Mechanism #br#
WU Yu, DENG Lunzhi, XU Kai, XUE Danni
2023, 20(6):  473-478.  doi:10.3870/j.issn.1672-8009.2023.06.002
Abstract ( 128 )   PDF (2926KB) ( 33 )  
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Objective To explore the protective effect of Oxysophocarpine (OSC) on myocardial ischemia-reperfusion injury in rat and the mechanism. Methods The cardiac function indicators were detected using echocardiography. The myocardial tissue lesions were observed using HE staining. The levels of heart injury markers and serum inflammatory factor were detected using ELISA methods. The oxidative stress markers were detected using corresponding reagent kits. Theexpression levels of related proteins were detected using Western bloting. Results Compared withthe sham group, the I / R group showed obvious myocardial injury, reduced cardiac function, and up-regulated levels of CK-Mb, Mb and cTnI. The serum level of SOD was significantly decreased, while that of MDA and LDH were increased. The levels of TNF-α, IL-1β, IL-6 and IL-10 were significantly increased, and the expression levels of p-ERK1 / 2 and p-JNK were significantly up-regulated. Compared with the I / R group, OSC treatment significantly improved myocardial injury and myocardial function. OSC treatment significantly inhibited myocardial oxidative stress and the release of pro-inflammatory factors. OSC treatment decreased p-ERK1 / 2 and p-JNK expressions.Conclusion OSC could improve cardiac dysfunction caused by I / R in rats, and inhibit oxidativestress and inflammatory responses. Its mechanism is related to the downregulation of ERK / JNK pathway.
CircPRKCI Regulates Proliferation, Apoptosis, Migration and Invasion of Esophageal Squamous Cell Carcinoma via miR-101-3p/TGFBR3 Axis #br#
MA Jun, GAO Yang, MA Yao, REN Mingzhi, ZHANG Tianyi
2023, 20(6):  479-486.  doi:10.3870/j.issn.1672-8009.2023.06.003
Abstract ( 65 )   PDF (7035KB) ( 44 )  
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Objective To explore the impact of circular RNA PRKCI (CircPRKCI) on malignant behavior of esophageal squamous cell carcinoma (ESCC) cells through the miR-101-3p / transforming growth factor beta type Ⅲ receptor ( TGFBR3) axis. Methods si-NC, si-CircPRKCI,miR-NC, miR-101-3p mimics, vector + miR-101-3p mimics, and CircPRKCI + miR-101-3p mimicswere transfected into KYSE150 cells, RT-qPCR was used to detect the mRNA expression levels ofCircPRKCI, miR-101-3p and TGFBR3 in cells. RT-qPCR, cell counting kit-8 (CCK-8) method,transwell assay, flow cytometry, and Western blotting were used to detect the malignant behavior ofcells in each group. Results CircPRKCI and TGFBR3 mRNA were upregulated and miR-101-3p expression was downregulated in KYSE150 cells (P < 0. 05). Silencing CircPRKCI was able to target and upregulate miR-101-3p and to inhibit TGFBR3 expression as well as cell viability, and cell invasive and migratory capacity, and to enhance the cell apoptosis (P < 0. 05). Up-regulation of miR- 101-3p significantly inhibited the malignant behavior of KYSE150 cells, whereas the overexpression of CircPRKCI attenuated the inhibitory effect of up-regulation of miR-101-3p on the malignant behavior of KYSE150 cells (P<0.05). Conclusion CircPRKCI can target and negatively regulate the miR-101-3p/TGFBR3 axis to affect malignant biological behavior such as proliferation, migration, invasion and apoptosis of ESCC cells.



Effect of Betulinic Acid on RANKL Induced Osteoblast Differentiation of MC3T3-E1 Cells and Its Mechanism #br#
LI Zongwei, WANG Jiahong, QING Quan
2023, 20(6):  487-492.  doi:10.3870/j.issn.1672-8009.2023.06.004
Abstract ( 49 )   PDF (2183KB) ( 39 )  
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Objective To observe the effect of betulinic acid ( BA) on receptor activator ofnuclear factor-κb ligand ( RANKL) induced osteoblast differentiation in preosteoblast cell line(MC3T3-E1), and to explore its possible mechanism. Methods MC3T3-E1 cells were cultured invitro with treatment of different concentrations (0, 5, 10, 20 μmol / L) of BA for 48 h. The proliferation of MC3T3-E1 was detected by CCK-8. Cells were divided into 5 groups. Control group, RANKL group, RANKL + BA group, RANKL + BA + 740Y-P (PI3K agonist) group and RANKL + BA + Curcumin (MEK / ERK agonist) group. The level of interleukin-6 (IL-6) in cell supernatant was detected by ELISA. The activity of alkaline phosphatase (ALP) was detected by ALP activity detection kit. The expression levels of osteocalcin (OCN), osteopontin (OPN), Collagen I, p-P65, P65, MEK / ERK and PI3K signaling pathway proteins were detected by Western blotting. Results BA of 5 μmol / L and 10 μmol / L was of no significant toxicity to MC3T3 cells. Thepretreatment with 10 μmol / L BA could significantly reduce the level of IL-6 and the ratio of p-P65 /P65 which were induced by RANKL (P < 0. 05). The down-regulation of OCN, OPN, Collagen I proteins induced by RANKL were significantly reversed by treatment of 10 μmol / L BA (P < 0. 05).10 μmol / L BA could obviously inhibit the phosphorylation of MEK, ERK and PI3K ( P < 0. 05). 10 μmol / L BA could significantly increase the expression levels of osteogenic marker proteins(OCN, OPN, Collagen I), and could increase the positive rate and activity of APL staining. Theabove effects were significantly weakened by the MEK / ERK agonist curcumin and PI3K agonist740Y-P (P< 0. 05). Conclusion BA can improve the inflammatory micro-environment by inhibiting NF-κB activation and IL-6 secretion, and can promote the osteoblast differentiation through inhibition of MEK / ERK and PI3K pathways.

Effect of Melatonin on Pulmonary Ischemia-reperfusion Injury in Diabetic Rats through JAK2 / STAT3 Signaling Pathway #br#
QU Yinhui, CHEN Congjie, WANG Lijuan
2023, 20(6):  493-499.  doi:10.3870/j.issn.1672-8009.2023.06.005
Abstract ( 42 )   PDF (2674KB) ( 149 )  
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Objective To investigate the effect of melatonin on lung ischemia / reperfusion (I /R) injury in diabetes mellitus ( DM) rats and its underlying molecular mechanism. Methods Rats were randomly divided into Control + Sham operation group (Control + Sham group), diabetes +Sham operation group ( DM + Sham group), Control + ischemia-reperfusion group ( Control + IRgroup), diabetes + ischemia-reperfusion group (DM + IR group), diabetes + ischemia-reperfusion +melatonin group (DM + IR + MT group), 8 rats in each group. The wet / dry weight ratio ( W / D)was measured in each group. Hematoxylin-eosin (HE) staining was used to detect the pathologicalchanges of lung tissues in each group. The activity of oxidative stress factor glutathione peroxidase(GSH-PX), superoxide dismutase ( SOD) and malondialdehyde ( MDA), and the level of totalantioxidant capacity (T-AOC) were detected in the lung tissues of rats in each group. The levels ofinflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) were detected by ELISA. The expression levels of p-JAK2 and p-STAT3 were detected by Western blotting. Results Compared with those in the Control + Sham group, the ratio of W/ D wasincreased, the alveolar septum and space edema, the interstitial thickening, and the alveolar hemorrhage and leukocyte infiltration were found, the lung injury score was higher, the activities of GSH-Px, SOD and T-AOC were decreased, and the level of MDA was increased, the levels of IL- 1β, IL-6 and TNF-a were increased, and the expression levels of p-JAK2 and p-STAT3 were increased in the Control + IR group (P< 0. 05). The above indexes were further increased in the DM+ sham group and the DM + IR group, and the difference was more significant in the DM + IR group. Compared with those in the DM + IR group, the ratio of W/ D was significantly decreased, the injuries in the lung tissue were significantly reduced, the lung injury score was decreased, the activities of GSH-Px, SOD and T-AOC were increased, and the level of MDA was decreased, the levels of IL-1β, IL-6 and TNF-α were decreased, and the expression levels of p-JAK2 and pSTAT3 were decreased in the DM + IR + ME group (P< 0. 05). Conclusion Melatonin attenuatedlung I / R injury the diabetic rats by reducing oxidative stress and inflammation, and its mechanism could be related to the JAK2 / STAT3 signaling pathway.

LncRNA ZFAS1 Targeting miR-34b-5p Regulates the Proliferation and Apoptosis of Diffuse Large B Cell Lymphoma Cells #br#
JIA Zhenwei, JIA Zhenheng , GUAN Jiangfeng , LI Yan
2023, 20(6):  500-505.  doi:10.3870/j.issn.1672-8009.2023.06.006
Abstract ( 49 )   PDF (3426KB) ( 47 )  
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Objective To investigate whether LncRNA ZFAS1 promotes proliferation and inhibit apoptosis in diffuse large B cell lymphoma (DLBCL) cell by regulating miR-34b-5p. Methods Real-time fluorescence quantitative PCR (RT-qPCR) was performed to detect the expression levels of LncRNA ZFAS1 and miR-34b-5p in tumor tissues of DLBCL patients and DLBCL cell lines. The vectors with or without the sequences for ZFAS1 knock-down and miR-34b-5p inhibition / overexpression were transfected into the SU-DHL-4 cells using Lipofectamine 2000 reagent. RTqPCR was performed to detect the knockdown and overexpression efficiency. The targeting relationship of ZFAS1 and miR-34b-5p was analyzed by dual luciferase reporter gene assay. SU-DHL-4 cells were then randomly grouped into control group, sh-ZFAS1 group, miR-34b-5p inhibitor group and shRNA-ZFAS1 + miR-34b-5p inhibitor group. Colony formation assay and flow cytometry were performed to detect cell proliferation and apoptosis, respectively. Western blotting assay was performedto detect the expression levels of apoptosis-related proteins. Results The expression level of ZFAS1 was increased in DLBCL patients and cell lines, while the expression level of miR-34b-5p was decreased. miR-34b-5p was targeted and negatively regulated by ZFAS1. The expression level of miR- 34b-5p was increased in the sh-ZFAS1 group and was decreased in the miR-34b-5p inhibitor group, when compared with those in the control group. The expression level of miR-34b-5p was higher in the sh-ZFAS1 + miR-34b-5p inhibitor group than that in the miR-34b-5p inhibitor group. Knockdown of ZFAS1 expression inhibited the proliferation, promoted the apoptosis, and decreased the mitochondrial membrane potential in SU-DHL-4 cells, while the Bax / Bcl-2 and cleaved-caspase-3 / caspase-3ratios were elevated. Conclusion LncRNA ZFAS1 promotes the proliferation and inhibits the apoptosis in SU-DHL-4 cells through down-regulation of miR-34b-5p.

Effect of LncRNA NEAT1 on Biological Activity of Lipopolysaccharide-induced Human Gingival Fibroblasts by Regulating miR-22-3p #br#
FAN Jing, GAO Yiman, ZHENG Yuan, GUO Danni, HU Jinlong, LEI Xiaopeng
2023, 20(6):  506-511.  doi:10.3870/j.issn.1672-8009.2023.06.007
Abstract ( 57 )   PDF (2108KB) ( 31 )  
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Objective To investigate the influence of long non-coding RNA ( LncRNA) nuclear-enriched abundant transcript 1 ( NEAT1) on the biological activity of human gingival fibroblasts (HGFs) induced by lipopolysaccharide (LPS) by regulating miR-22-3p. Methods HGFs cells in logarithmic growth phase were grouped into 6 groups: control group, LPS group, si-NC group, si-Neat1 group, si-Neat1 + inhibitor NC group, and si-Neat1 + miR-22-3p inhibitor group. RT-qPCR was applied to detect the expression levels of Neat1 and miR-22-3p. Dual luciferase reporter assay was applied to verify the targeting relationship of Neat1 and miR-22-3p. Flow cytometry, CCK-8, and ELISA were used to detect apoptosis, cell viability, and levels of tumor necrosis factor-α (TNF-α) and interleukin-1β ( IL-1β), respectively. Western blotting assay was applied to detect the expression levels of caspase-3and NF-κB P65, and the phosphorylation level of NF-κBP65 (p-NF-κB P65). Results The cell viability and the expression level of miR-22-3p in the LPSgroup were significantly decreased, while the TNF-α, IL-1β, apoptosis rate, the levels of p-NF-κB P65 / NF-κB P65, Neat1, and Caspase-3 were significantly increased (P < 0. 05), when compared with those in the control group. The cell viability and the expression level of miR-22-3p in the si-Neat1 group were significantly increased, while the TNF-α, IL-1β, apoptosis rate, the levels ofp-NF-κB P65 / NF-κB P65, Neat1and Caspase-3 were significantly decreased ( P < 0. 05), when compared with those in the LPS group and the si-NC group. Down-regulation of miR-22-3p expression reversed the effect of Neat1 silencing on the biological activity of LPS-induced HGFs ( P <0. 05). Conclusion Silencing Neat1 can inhibit the apoptosis and inflammatory response of HGFsinduced by LPS, the mechanism may be related to the up-regulation of miR-22-3p expression.
Gastrodin Promotes Autophagy in Osteoarthritis Chondrocytes by Regulation of AMPK / mTOR Pathway #br#
ZHANG Yu, CHEN Jingyou
2023, 20(6):  512-518.  doi:10.3870/j.issn.1672-8009.2023.06.008
Abstract ( 37 )   PDF (2515KB) ( 39 )  
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Objective To investigate the effect of gastrodin ( GSTD) on the autophagy of chondrocytes in osteoarthritis and its mechanism. Methods The effect of GSTD on the chondrocyteviability was detected by CCK-8 assay. Chondrocytes were stimulated with IL-1β (10 ng / mL) to establish the osteoarthritis cell injury model in vitro. Cells were divided into 3 groups: control group,IL-1β group, and IL-1β + GSTD group. The apoptosis rate was detected by flow cytometry after 48 h culture. Western blotting was used to detect the expression levels of autophagy related proteins (LC3 and P62), AMPK, and mTOR. The secretion levels of COL2A1, MMP-13, TNF-α, and IL-6 in cell culture supernatant were determined by enzyme-linked immunosorbent assay ( ELISA). AMPK inhibitor (compound C) was used to observe the role of AMPK pathway in chondrocyte autophagy. Results GSTD treatment increased cell viability in the range of 12. 5 ~ 50 μmol / L. Cells pretreated with 25 μmol / L GSTD were selected for the subsequent experiments. IL-1β stimulated cellsto promote chondrocyte apoptosis (P < 0. 05), inhibited autophagy (P < 0. 05), increased the secretion of inflammatory factors (P < 0. 05), inhibited the expression level of COL2A1 and increased the expression level of MMP-13 (P < 0. 05), when compared with the control group. Compared with the cells in the IL-1β group, cells in the GSTD pretreated group had increased autophagy ( P <0. 05), decreased apoptosis ( P < 0. 05), decreased levels of inflammatory cytokines, decreasedexpression level of MMP-13 and phosphorylation of mTOR ( P < 0. 05), and increased expressionlevel of COL2A1 (P< 0. 05) and phosphorylation of AMPK. Treatment of cells with AMPK pathwayinhibitor (compound C) reversed the protective effect of GSTD on chondrocytes, resulting in thedecrease in apoptosis ratio, autophagy level and expression level of COL2A1, and the increased insecretion of inflammatory factors and expression level of MMP-13 (P < 0. 05). Conclusion GSTDpromotes the chondrocytes autophagy through the regulation of AMPK / mTOR signaling pathway,and protects chondrocytes from apoptosis and inflammatory response and by promotion of collagensynthesis.
Effect of KIF20A Gene on Radiosensitivity of Huh7 Liver Cancer Cells and Its Mechanism #br#
WANG Chao, YANG Jianrui, LI Zhijun, WU Lin, ZHANG Jun
2023, 20(6):  519-524.  doi:10.3870/j.issn.1672-8009.2023.06.009
Abstract ( 66 )   PDF (5265KB) ( 53 )  
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Objective To investigate the effect of kinesin family member 20A (KIF20A) gene on the radiosensitivity of hepatocellular carcinoma cells Huh7 and its possible mechanism. Methods RT-qPCR was used to detect the expression levels of KIF20A mRNA in Huh7 after irradiation with different doses (0, 2, 4, 6, 8 Gy). The Huh7 cell line with silenced expression of KIF20A was constructed by lentivirus transduction. The efficiency of RNA silencing on KIF20A was verified byRT-qPCR and Western blotting, cell survival was detected by cell counting kit 8 ( CCK-8) and colony formation assay, apoptosis was detected by flow cytometry, cell invasion and migration were detected by transwell assay and wound-healing assay, and the expression levels of PI3K / AKT signaling pathway-related proteins were detected by Western blotting. Results The mRNA expression level of KIF20A in Huh7 cells was increased with the treatment of increased X-ray dose ( P < 0. 05). KIF20A knockdown significantly inhibited the expression levels of KIF20A mRNA and protein in Huh7 cells (P< 0. 05). With the treatment of increased radiation dose, the cell survival rate decreased gradually (P< 0. 05), the survival rate of Huh7 cells with KIF20A silencing was further decreased (P< 0. 05). The colony formation rate of Huh7 cells with KIF20A silencing was significantly decreased (P< 0. 05), the invasion and migration ability were significantly inhibited (P < 0. 05), the apoptosis rate was significantly increased (P < 0. 05), the level of PI3K in cells was down-regulated (P < 0. 05 ) and the level of AKT phosphorylation was decreased ( P < 0. 05 ). Conclusion Silencing KIF20A can enhance the radiosensitivity of Huh7 liver cancer cells, and its mechanism may be related to the PI3K / AKT signaling pathway.

Advances in Research on Regulation of Tuberculous Pleural Fibrosis by Growth Factor #br#
REN Shangxian, JIANG Shenghua
2023, 20(6):  525-529.  doi:10.3870/j.issn.1672-8009.2023.06.010
Abstract ( 48 )   PDF (674KB) ( 47 )  
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Pleural fibrosis occurs during the recovery phase of tuberculous pleurisy and is oftenprogressive and irreversible, resulting in restricted ventilation dysfunction that significantly affects the quality of life. Therefore, early assessment of the disease and inhibition of the progression of pleural fibrosis are ways for the treatment of tuberculous pleurisy in the future. Although the regulatory mechanism of tuberculous pleural fibrosis has not been systematically elucidated, relevant studies have shown that many important growth factors are involved in the occurrence and development of tuberculous pleural fibrosis. The involved growth factors mainly include transforming growth factor beta (TGF-β), vascular endothelial growth factor ( VEGF), platelet-derived growth factor ( PDGF), fibroblast growth factor (FGF), connective tissue growth factor (CTGF), hepatocyte growth factor (HGF). This article reviews the research progress of tuberculous pleurisy and tuberculous pleural fibrosis, as well as the expression of TGF-β, VEGF, PDGF, FGF and CTGF in tuberculous pleural fibrosis and their possible regulatory mechanisms.
Rho GTPase during Angiogenesis #br#
SHI Weili, GAO Haixia, WU Hong,
2023, 20(6):  530-535.  doi:10.3870/j.issn.1672-8009.2023.06.011
Abstract ( 29 )   PDF (1385KB) ( 53 )  
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Ischemic cardiovascular and cerebrovascular diseases are still the first killer that affecting health of Chinese residents. Angiogenesis participates in the repair process of tissue lesion after ischemia, and provides an effective method for the treatment of ischemic cardiovascular and cerebrovascular diseases. Rho GTPase family plays a central role in the regulation of endothelial cytoskeleton morphology, migration and tubulogenesis. Cdc42, Rac1 and RhoA, which are members of the Rho GTPase family, have been found to be involved in the angiogenesis. Cdc42 induces endothelial filopodia formation and directs endothelial migration, promotes the recovery of damaged vascular endothelial barrier. Rac1 controls the formation of lamellar pseudopodia. RhoA regulates the formation of focal adhesions, and dynamic remodeling of anterior and posterior matrix adhesion during endothelial migration. Cdc42, Rac1 and RhoA cooperatively participate in the angiogenesis after ischemic injury. Although the roles of Rho GTPase in angiogenesis have not been fully understood, the prospects of which from basic research to clinical application are still worth exploring, which is of great significance for the prevention and treatment of ischemic cardiovascular and cerebrovascular diseases.
Advances in Research on FKBPL in Diseases #br#
HOU Jingwen, WANG Xiaoyu, ZHAN Tian, WANG Aiyuan
2023, 20(6):  536-539.  doi:10.3870/j.issn.1672-8009.2023.06.012
Abstract ( 66 )   PDF (817KB) ( 50 )  
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FK506-binding protein like ( FKBPL) is a member of the immunophilin family,and its functions are highly diverse. It can regulate the signal transduction of steroid receptors, inhibit the growth of tumor stem cells and tumor cells, and serve as a biological marker for tumor prognosis. Recent research has revealed the presence of an anti-angiogenesis domain in the N-terminal region of FKBPL, indicating its role in regulating angiogenesis both in vivo and in vitro. Additionally, FKBPL is associated with various issues such as inflammation, ocular diseases,and psychological disorders. This review aims to make a summary of the recent researches on FKBPL from the aspects of its structure and functions, and discusses its potential clinical applications.
Molecular Structure of Epigenetics Reader Morc3 and Its Role in Disease Development #br#
FU Wenxuan, SHI Yan,
2023, 20(6):  540-546.  doi:10.3870/j.issn.1672-8009.2023.06.013
Abstract ( 44 )   PDF (816KB) ( 44 )  
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MORC3 is an important member of the MORC nuclear protein superfamily. It is a genetic regulatory factor, which is often related to the occurrence of autoimmune diseases and cancer. In recent years, with the rapid development of molecular research technology, researches on the MORC3 molecular structure has also become a hot spot. Among them, the zinc finger structure and the ATP enzyme domain of MORC3 have attracted wide attention, and its immune regulatory effect has also been discovered. In addition, more and more studies have shown that MORC3 plays a diverse and irreplaceable role in the human body. This article mainly introduces the molecular structure and function of MORC3 and its role in regulation of genetic materials, and its participation in the development of diseases.