Objective To explore the effects of glycyrrhizic polysaccharide(GP)on the biological activity of salivary adenoid cystic carcinoma tumor cells and its mechanisms of anti-tumor action.Methods GP was prepared,and human adenoid cystic carcinoma high-metastatic cell line SACC-LM and low-metastatic cell line SACC-83 were used as target cells.Different concentrations of GP were used for intervention.The cell counting kit-8(CCK-8)assay was employed to detect cell proliferation and apoptosis.Reverse transcrip-tion polymerase chain reaction(RT-PCR)and Western blot experiments were conducted to detect the expression of genes and proteins related to tumor invasion and metastasis.The scratch assay was used to observe the effect of GP on the migration ability of SACC cells.In vivo experiments were conducted to verify the inhibitory effect of GP on tumor cells.Results Glycyrrhiza polysaccharides signifi-cantly inhibited the proliferation and migration of the highly metastatic human adenoid cystic carcinoma cell line SACC-LM by regulating the expression of epithelial-mesenchymal transition(EMT)-related markers.In vivo experiments showed that glycyrrhiza poly-saccharides had no significant hepatotoxicity,could significantly reduce the volume and weight of tumors,and inhibit the growth rate of tumors in nude mice.Conclusion GP has a certain inhibitory effect on the growth and migration ability of SACC.

AIM:To explore the role of stromal interaction molecule 1(STIM1)in the migration,invasion and angiogenesis of salivary adenoid cystic carcinoma(SACC),as well as its molecular mechanism.METHODS:Immu-nohistochemistry and Western blot were used to detect the expression level of STIM1 in human SACC tumor tissues and ad-jacent normal tissues.The TCGA database was analyzed to investigate the relationship between STIM1 expression and sur-vival in patients.A SACC-83 cell line with stable STIM1 overexpression(STIM1-OE)was established and divided into two groups:blank control(STIM1-Vec)group and STIM1-OE group.A nude mouse subcutaneous xenograft tumor model(n=6)was used to detect SACC growth.Transwell chamber assay,scratch test and dorsal root ganglion model were ap-plied to assess SACC migration and invasion.Immunohistochemistry was performed to detect the expression of CD34 and STIM1 in tumor tissues of nude mice.A nude mouse Matrigel plug model and human umbilical vein endothelial cell(HUVEC)tube formation assay were used to evaluate angiogenesis.Enzyme linked immunosorbent assay was employed to detect the levels of vascular endothelial growth factor(VEGF)and epidermal growth factor(EGF)in cell culture supernatants.RT-qPCR and Western blot were performed to detect the mRNA and protein expression levels of c-Myc,ribosomal protein L35(RPL35),ribosomal protein SA(RPSA),mitochondrial ribosomal protein L11(RPL11)and FAU ubiquitin like and ribo-somal protein S30 fusion(FAU).The STIM1-siRNA and RPL35-siRNA were transfected into SACC-83 cells,and the mi-gration,invasion and angiogenesis abilities of the cells were detected using the same methods as above.RESULTS:STIM1 was highly expressed in SACC,and the patients with high STIM1 expression had shorter survival time.In vivo,compared with STIM1-Vec group,STIM1-OE promoted tumor growth.In vitro,the number of migrating and invading SACC cells in STIM1-OE group was significantly increased,and the nerve invasion ability was also significantly en-hanced.Conversely,STIM1-siRNA significantly reduced the migration and invasion abilities of SACC cells.Additional-ly,STIM1-OE significantly promoted the expression of the vascular marker CD34,the secretion of VEGF and EGF,and the results of Matrigel plug and HUVEC tube formation assays indicated that STIM1-OE significantly promoted angiogene-sis.Silencing of RPL35 significantly inhibited SACC migration,invasion,and angiogenesis.RT-qPCR and Western blot results showed that the mRNA levels of RPL35,RPSA,MRPL11 and FAU were significantly increased(P<0.05),and the protein expression levels of STIM1,c-Myc and RPL35 were significantly increased(P<0.01).CONCLUSION:STIM1 drive the migration,invasion and angiogenesis of SACC by activating c-Myc/RPL35-mediated ribosome pathway.

Objective To explore the effects of glycyrrhizic polysaccharide(GP)on the biological activity of salivary adenoid cystic carcinoma tumor cells and its mechanisms of anti-tumor action.Methods GP was prepared,and human adenoid cystic carcinoma high-metastatic cell line SACC-LM and low-metastatic cell line SACC-83 were used as target cells.Different concentrations of GP were used for intervention.The cell counting kit-8(CCK-8)assay was employed to detect cell proliferation and apoptosis.Reverse transcrip-tion polymerase chain reaction(RT-PCR)and Western blot experiments were conducted to detect the expression of genes and proteins related to tumor invasion and metastasis.The scratch assay was used to observe the effect of GP on the migration ability of SACC cells.In vivo experiments were conducted to verify the inhibitory effect of GP on tumor cells.Results Glycyrrhiza polysaccharides signifi-cantly inhibited the proliferation and migration of the highly metastatic human adenoid cystic carcinoma cell line SACC-LM by regulating the expression of epithelial-mesenchymal transition(EMT)-related markers.In vivo experiments showed that glycyrrhiza poly-saccharides had no significant hepatotoxicity,could significantly reduce the volume and weight of tumors,and inhibit the growth rate of tumors in nude mice.Conclusion GP has a certain inhibitory effect on the growth and migration ability of SACC.

AIM:To explore the role of stromal interaction molecule 1(STIM1)in the migration,invasion and angiogenesis of salivary adenoid cystic carcinoma(SACC),as well as its molecular mechanism.METHODS:Immu-nohistochemistry and Western blot were used to detect the expression level of STIM1 in human SACC tumor tissues and ad-jacent normal tissues.The TCGA database was analyzed to investigate the relationship between STIM1 expression and sur-vival in patients.A SACC-83 cell line with stable STIM1 overexpression(STIM1-OE)was established and divided into two groups:blank control(STIM1-Vec)group and STIM1-OE group.A nude mouse subcutaneous xenograft tumor model(n=6)was used to detect SACC growth.Transwell chamber assay,scratch test and dorsal root ganglion model were ap-plied to assess SACC migration and invasion.Immunohistochemistry was performed to detect the expression of CD34 and STIM1 in tumor tissues of nude mice.A nude mouse Matrigel plug model and human umbilical vein endothelial cell(HUVEC)tube formation assay were used to evaluate angiogenesis.Enzyme linked immunosorbent assay was employed to detect the levels of vascular endothelial growth factor(VEGF)and epidermal growth factor(EGF)in cell culture supernatants.RT-qPCR and Western blot were performed to detect the mRNA and protein expression levels of c-Myc,ribosomal protein L35(RPL35),ribosomal protein SA(RPSA),mitochondrial ribosomal protein L11(RPL11)and FAU ubiquitin like and ribo-somal protein S30 fusion(FAU).The STIM1-siRNA and RPL35-siRNA were transfected into SACC-83 cells,and the mi-gration,invasion and angiogenesis abilities of the cells were detected using the same methods as above.RESULTS:STIM1 was highly expressed in SACC,and the patients with high STIM1 expression had shorter survival time.In vivo,compared with STIM1-Vec group,STIM1-OE promoted tumor growth.In vitro,the number of migrating and invading SACC cells in STIM1-OE group was significantly increased,and the nerve invasion ability was also significantly en-hanced.Conversely,STIM1-siRNA significantly reduced the migration and invasion abilities of SACC cells.Additional-ly,STIM1-OE significantly promoted the expression of the vascular marker CD34,the secretion of VEGF and EGF,and the results of Matrigel plug and HUVEC tube formation assays indicated that STIM1-OE significantly promoted angiogene-sis.Silencing of RPL35 significantly inhibited SACC migration,invasion,and angiogenesis.RT-qPCR and Western blot results showed that the mRNA levels of RPL35,RPSA,MRPL11 and FAU were significantly increased(P<0.05),and the protein expression levels of STIM1,c-Myc and RPL35 were significantly increased(P<0.01).CONCLUSION:STIM1 drive the migration,invasion and angiogenesis of SACC by activating c-Myc/RPL35-mediated ribosome pathway.

OBJECTIVE To investigate the ameliorative effects and mechanism of Sanwei ganlu on hepatic fibrosis in rats. METHODS The rats were randomly divided into normal group， model group， silibinin group （positive control， 50 mg/kg）， and Sanwei ganlu low-dose， medium-dose， and high-dose groups （80， 250， 800 mg/kg）. Except for normal group， hepatic fibrosis rat models were established by intraperitoneal injection of CCl4 in the other groups of rats. Starting from the 6th week of modeling administration， they were given normal saline or corresponding drugs intragastrically at the same time. At the end of the ninth-week experiment， liver and spleen indexes of rats were calculated； the pathological structure and fibrosis changes of liver tissue were observed by HE， Masson and Sirus Red staining. The contents of alanine transaminase （ALT）， aspartate transaminase （AST）， procollagen type Ⅲ （PC Ⅲ）， collagen type Ⅳ （COL-Ⅳ）， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α） and IL-1β in serum， and hyaluronic acid （HA） and laminin （LN） in liver tissue were all detected. RESULTS Compared with the model group， the liver injury and collagen fiber deposition of rats were improved to different extents in Sanwei ganlu groups and silibinin group； the contents of ALT， AST， PC Ⅲ， COL-Ⅳ， IL-6， TNF-α and IL-1β in serum as well as the contents of HA and LN in liver tissue significantly decreased （P＜0.05 or P＜0.01）. CONCLUSIONS Sanwei ganlu can alleviate the progression of hepatic fibrosis in rats， possibly by inhibiting the synthesis of collagen fiber， reducing transaminase content， down-regulating the levels of HA， LN， PC Ⅲ and COL-Ⅳ， and reducing the inflammatory response.

Objective: To investigate the effect of adding glutathion(GSH) to tumescent solution on autologous fat graft survival. Methods: 14 male and female New Zealand rabbits were divided into experimental group and control group randomly, 7 in each group. Experimental group: The donor areas of the rabbits were injected with 3 ml of tumescent solution with GSH. Control group: The donor areas of the rabbits were injected with 3 ml regular tumescent solution. DCFH-DA probe was used for fluorescent staining of harvested fat cells. Then stained fat cells were measured for the intracellular reactive oxygen species(ROS)content by fluorescence microplate. The grafts were harvested at 3 months after transplantation and assessed by general observation, volume measurement, wet weight measurement, HE staining for the number of fat cells, and CD34 immunohistochemical staining for the measurement of micro-vascular density. T test was performed by using SPSS 24.0. Results: The intracellular ROS content of harvested fat cells in experimental group was lower than that in control group, and the difference was statistically significant (P<0.05). At 3 months after transplantation, the wet weight of fat grafts in experimental group was (1133.21±87.97) mg and that in control group was (718.79±79.27) mg. The volume of fat grafts in experimental group was (1.00±0.04) ml and that in control group was (0.59±0.03) ml. The number of fat cells in experimental group was (746.6±15.7)/10 high magnification vision and that in control group was (350.1±32.4)/10 high magnification vision. The density in group experimental was (8.1±2.0)/high magnification vision and that in control group was (6.7±2.4)/high magnification vision. The grafts′ volume, wet weight, and the number of fat cells in experimental group were higher than those in control group, and the differences were statistically significant (P<0.05). The difference of micro-vascular density between experimental group and control group had no statistical significance (P>0.05). Conclusions The addition of GSH to tumescent solution optimizes the process of autologous fat harvest, thereby improving the survival of fat graft.