Objective： To investigate the expression of K-ras in human laryngeal squamous cell carcinoma cell lines （Hep-2） and its significance for establishing a solid foundation for further study of the relationship between...Objective： To investigate the expression of K-ras in human laryngeal squamous cell carcinoma cell lines （Hep-2） and its significance for establishing a solid foundation for further study of the relationship between human laryngeal squamous cell carcinoma and K-ras gene point mutations. Methods： The expression of K-ras in human laryngeal squamous cell carcinoma cell lines （Hep-2） and human pancreatic carcinoma cell lines （MIAPaCa-2） was detected by using RT-PCR. Results： The expression of K-ras mRNA in Hep-2 and MIAPaCa-2 was strong and positive. Conclusion： The expression of K-ras mRNA in human laryngeal squamous cell carcinoma cell lines （Hep-2） is positive. Development of laryngeal carcinoma might be related to the activation of K-ras gene point mutation.展开更多
Objective： To investigate the effects of 5-Aza-2＇-deoxycytidine （5-Aza-Cdr） and trichostatin A （TSA） combined with p53-expressing adenovirus （Ad-p53） on Hep-2 cell line in vivo and in vitro, in order to explor...Objective： To investigate the effects of 5-Aza-2＇-deoxycytidine （5-Aza-Cdr） and trichostatin A （TSA） combined with p53-expressing adenovirus （Ad-p53） on Hep-2 cell line in vivo and in vitro, in order to explore its possibility in biological treatment of laryngocarcinoma. Methods： Effects of 5-Aza-Cdr and TSA in combination with Ad-p53 on Hep-2 cell line in vivo were determined by Cell Counting Kit-8 （CCK-8） assay. The effect of drug combination was calculated by Jin＇s formula. Effects on the cell line in vitro were investigated by establishing the nude mice model. Results： 5-Aza-Cdr and TSA showed inhibitory effects on the proliferation of Hep-2 cells in dose- and time-dependent manner. Ad-p53 can inhibit the growth of Hep-2 cells in vivo and in vitro. However, the combination of epigenetic reagents （5-Aza-Cdr/TSA） and Ad-p53 was less effective than individual use of Ad-p53. 5-Aza-Cdr and Ad-p53 inhibited the growth of transplanted tumors and reduced the volume of tumors, and the tumor volume of Ad-p53 group was significantly smaller than that of the control group （P0.05）. Conclusion： Both epigenetic reagents （5-Aza-Cdr/TSA） and Ad-p53 can suppress cell proliferation on Hep-2 in vivo and in vitro and there may be some antagonistic mechanism between Ad-p53 and epigenetic reagents （5-Aza-Cdr/ TSA）.展开更多
Objective：The aim of this study was to investigate the af ecting of Rg3 to secreted VEGF of human laryngeal carcinoma Hep-2 cells and its mechanism of inhibition to tumor angiogenesis. Methods：Cultured human larynge...Objective：The aim of this study was to investigate the af ecting of Rg3 to secreted VEGF of human laryngeal carcinoma Hep-2 cells and its mechanism of inhibition to tumor angiogenesis. Methods：Cultured human laryngeal cancer cellline Hep-2 and human vascular endothelial cells in vitro, cells got into the period of exponential phase of growth, was diviced into 3 groups：group I （control group）, group II （DDP group）, group III （Rg3 group）. Added to the Hep-2 cells Rg3 and DDP, made Rg3 final concentration was 300μg/mL, and DDP was 3μg/mL. 48 h later, specimens from sample to be done immunocytochemistry, and the protein of VEGF in Hep-2 cells to be detected. Col ecting Hep-2 cells supernatant, some was used to measure the protein level of VEGF in Hep-2 cells supernatant by ELISA. Some was used to culture HVEC. 24 h later, cellgrowth inhibition rate of human vascular endothelial was determined by MTT. Results：The protein level of VEGF was evi-dently higher in group I compared to group II and group III, it was not only in Hep-2 cells, but also in supernatant of Hep-2 cells. There was no significantly dif erent between group II and group III. MTT results showed that, the human vascular endothelial cellgrowth inhibition rate of group I was significantly lower than that of group II and group III （P〈0.05）. At the same time the HVEC growth inhibition rate of group II was significantly lower than that of group III （P〈0.05）. Conclusion：The inhibition to tumor angiogenesis of Rg3 is stronger than traditional chemotherapy drug cisplatin. It worke by reducing the biological ef ects of secreted VEGF, But the ef ecting worke by reducing the activity of secreted VEGF itself or af ecting endothelial function of VEGF receptor or some other ways to be further studied.展开更多
Objective： The aim of the study was to establish models of Hep-2 laryngeal cancer cell line of different oxygen supplying, trying to investigate the impact of normoxia, hypoxia, reoxygenation after hypoxia on apoptos...Objective： The aim of the study was to establish models of Hep-2 laryngeal cancer cell line of different oxygen supplying, trying to investigate the impact of normoxia, hypoxia, reoxygenation after hypoxia on apoptosis and expression of proteins HIF-1α and p53 to Hep-2 human laryngeal cancer cell line induced by ^60Co γ-ray. Methods： Human laryngeal cancer Hep-2 cells were divided into 3 groups： group A （normoxia）, group B （hypoxia）, and group C （reoxygenation after hypoxia）. All of the cells were exposed to 5 Gy dosage of γ-ray. Flow cytometry （FCM） was used tomeasure the protein levels of HIF-1α and p53 and to detect cell apoptosis. The protein levels of HIF-la and p53 were also determined by immunohistochemistry and Western blotting. The expression of HIF-la mRNA was determined by RT-PCR. Results： The protein levels of HIF-1α and p53 were evidently increased in group B compared to group A. The protein levels of HIF-1α and p53 in group C were lower compared to group B; the rate of apoptosis in group C was higher than that in group B. Conclusion： Hypoxia decreased the effect of apoptosis induced by ^60Co γ-ray in Hep-2 human laryngeal cancer cell line. The apoptosis pathway maybe related to some other genes or proteins but not p53 in the conditions of hypoxia and reoxygenation after hypoxia.展开更多
Objective： The aim of the study was to investigate the impact of 60Co y-ray on apoptosis, cell cycles and the expression of protein hypoxia-inducible factor-1α （HIF-1α） to Hep-2 cell line in the conditions of nor...Objective： The aim of the study was to investigate the impact of 60Co y-ray on apoptosis, cell cycles and the expression of protein hypoxia-inducible factor-1α （HIF-1α） to Hep-2 cell line in the conditions of normoxia and hypoxia. Methods： Hep-2 cell were divided into 2 groups： group A （normoxia） and group B （hypoxia）. All of the ceils were exposed to y-ray with dosage being 0, 1, 3, 5, 10, 20, and 40 Gy. Flow cytometry was used to measure the protein level of HIF-1α and to detect apoptosis and cell cycles. The protein level of HIF-1α was also determined by immunohistochemistry and Western blotting. Results： The protein level of HIF-1α in group B was significantly higher than that in group A. In group A, low doses （1-5 Gy） of y-ray had caused G0/G1 cell cycle arrest and high doses （10-40 Gy） had caused G2/M cell cycle arrest. In group B, without exposure of y-ray （0 Gy） had caused G0/G1 cell cycle arrest, all of the different dosage of y-ray could cause G2/M cell cycle arrest. The curve of apoptosis rate in group A was a parabola, the apoptotic rate was related to the dosage of y-ray in a dosage dependent manner. The peak was at the point of 5 Gy. The apoptosis rate in group A was significantly higher than that in group B. Conclusion： Different doses of y-ray could cause different cell cycles arrest then make different impact on apoptosis to Hep-2 ceil. The lower apoptosis rate in condition of hypoxia maybe has a relationship with G2/M cell cycle arrest. Up-regulated HIF-1α protein may be one of the reasons for G2/M cell cycle arrest.展开更多
In order to study the effect of 5, 6-Dichloro-l-13-D-ribofuranosyl-benzimidazole （DRB） on the biological characteristics of human laryngeal carcinoma Hep-2 cell line in vitro, Hep-2 cells cultured in vitro were trea...In order to study the effect of 5, 6-Dichloro-l-13-D-ribofuranosyl-benzimidazole （DRB） on the biological characteristics of human laryngeal carcinoma Hep-2 cell line in vitro, Hep-2 cells cultured in vitro were treated with different concentrations of DRB. Changes in cell proliferation, apoptotic rate and invasiveness were detected by MTT assay, flow cytometry （FCM） and matrigel in vitro invasion assay, respectively. It was found that DRB inhibited the proliferation of Hep-2 cells in a dose- and time-dependent manner. After being treated with 0, 10, 20, 40, 80 μmmol/L DRB for 24 h, the apoptotic rate in Hep-2 cells was （0.68±0.19）%, （1.95±0.12）%, （8.51±0.26）%, （11.26±0.17）% and （14.99±0.32）%, respectively. The matrigel in vitro invasion assay revealed that DRB began to inhibit the invasion of Hep-2 cells at the concentration of 5 μmmol/L, and with the increase of DRB concentration, the inhibitory effect was enhanced. It was suggested that DRB could influence the essential biological characteristics of Hep-2 cells, inhibit Hep-2 cells proliferation, reduce invasive ability and induce apoptosis of Hep-2 cells.展开更多
Summary: The inhibitory effects of two kinds of selective cyclooxygenase-2 inhibitors on the proliferation of human carcinoma of larynx Hep-2 in vitro and their corresponding mechanisms were investigated. Hep-2 cells ...Summary: The inhibitory effects of two kinds of selective cyclooxygenase-2 inhibitors on the proliferation of human carcinoma of larynx Hep-2 in vitro and their corresponding mechanisms were investigated. Hep-2 cells were cultured with two kinds of selective cyclooxygenase-2 inhibitors (Sc-58125 and Celecoxib) at various concentrations for 24 h. Morphological changes were observed under the phase microscopy and the growth suppression was detected by using MTT colorimetric assay. Apoptotic DNA fragments were observed by agarose gel electrophoresis, and the cell cycle and apoptotic rate were detected by flow cytometry (FCM) respectively. Hep-2 cells became rounded and detached from the culture dish after being treated with Celecoxib for 24 h, however, they remained morphologically unchanged with Sc-58125. Sc-58125 could increase G 2 phase cells, whereas, Celecoxib rose G 1 phase cells. Both of the two effects were dose-dependent. Moreover, the Hep-2 cells cultured with 50 μmol/L and 100 μmol/L Celecoxib showed obvious apoptosis, with the nuclear DNA of cells exhibiting characteristic DNA ladder. So Sc-58125 could inhibit the proliferation of Hep-2 cells by altering the G 2 phase cells. However, Celecoxib had the same effect by changing the G 1 phase cells and inducing apoptosis at higher concentration.展开更多
Objective To develop an improved substrate for indirect immunofluorescence test (IIF) for detecting anti-Ro60/Sjogren's syndrome A (Ro/SSA) autoantibodies.Methods 60-kDa Ro/SSA autoantigens (Ro60) cDNAs were obtai...Objective To develop an improved substrate for indirect immunofluorescence test (IIF) for detecting anti-Ro60/Sjogren's syndrome A (Ro/SSA) autoantibodies.Methods 60-kDa Ro/SSA autoantigens (Ro60) cDNAs were obtained from human placental cDNA library using polymerase chain reaction (PCR) and were cloned into the mammalian expression vector-pEGFP-C1. Then, the recombinant plasmids were transfected into HEp-2 cells. We confirmed the overexpression, localization and antigenicity of fusion proteins in transfected cells by means of immunoblotting, confocal fluorescence microscopy and IIF. HEp-2 and HEp-Ro60 were analyzed by IIF using a panel of 10 precipitin-positive anti-Ro human sera simultaneously.Results Stable expression of Ro60-green fluorescent protein (Ro60-GFP) fusion proteins were maintained ten more generations. Ro60-GFP kept the antigenicity of Ro while demonstrating its own characteristic immunofluorescent pattern in HEp-Ro60 cells. The transfectants dramatically increased the sensitivity of IIF testing (a mean increase of 6.7-fold in endpoint titer). Eight overten (8/10) positive anti-Ro sera showed characteristic immunofluorescent patterns for HEp-Ro60, including two sera that were anti-nuclear antibodies (ANA) negative for untransfected HEp-2. IIF-ANA in all healthy sera was negative for HEp-Ro60. Conclusions As a new substrate for IIF, the Ro60 transfectants can be used to detect anti-Ro antibodies. In addition, transfected HEp-2 cells keep the immunofluorescent properties of HEp-2 cells in IIF-ANA tests and can be employed as a substrate for routine IIF-ANA detection.展开更多
Bee venom （BV） was used from long time ago in the medical field as treatment of chronic joint affections. In the recent decades, the screening process of new sources of antimicrobials discovers its high advantageous...Bee venom （BV） was used from long time ago in the medical field as treatment of chronic joint affections. In the recent decades, the screening process of new sources of antimicrobials discovers its high advantageous characteristics for combating various types of microbes, as well as trials to discover its anti-cancer medicinal fields. Lumpy skin disease virus （LSDV） causes disease in cattle of economic importance, and this work aimed to find treatment as well as alternative inactivant for LSDV. The use of bee venom as antiviral was experimented in this work and exhibited satisfied inhibitory effects on LSDV, meanwhile, the antigenic properties was still intact. The viability of virus was tested in tissue culture cells lines and in embryonated chicken eggs. According to doses and time of exposure, the cell lines of Hep-2 （human larynx carcinoma） and MCF7 （breast carcinoma cell line） were treated with different concentrations of BV and examined after 24 h post-inoculation. The Hep-2 and MCF7 cell lines were treated with various concentrations of BV in descending doses as follow： 25, 20, 15, 10, 5 and 0.5 ug/mL of BV. Then bee venom pathological effects on Hep-2 cells and MCF7 cells were observed, such as apoptosis, retarded growths and cytolysis. The results indicate the possibilities of using bee venom as anti-neoplastic and antiviral.展开更多
基金This work was supported by a grant from the National Natural Science Foundation of China(No. 30070809).
文摘Objective： To investigate the expression of K-ras in human laryngeal squamous cell carcinoma cell lines （Hep-2） and its significance for establishing a solid foundation for further study of the relationship between human laryngeal squamous cell carcinoma and K-ras gene point mutations. Methods： The expression of K-ras in human laryngeal squamous cell carcinoma cell lines （Hep-2） and human pancreatic carcinoma cell lines （MIAPaCa-2） was detected by using RT-PCR. Results： The expression of K-ras mRNA in Hep-2 and MIAPaCa-2 was strong and positive. Conclusion： The expression of K-ras mRNA in human laryngeal squamous cell carcinoma cell lines （Hep-2） is positive. Development of laryngeal carcinoma might be related to the activation of K-ras gene point mutation.
基金supported by the National Natural Science Foundation of China (No.30772407)
文摘Objective： To investigate the effects of 5-Aza-2＇-deoxycytidine （5-Aza-Cdr） and trichostatin A （TSA） combined with p53-expressing adenovirus （Ad-p53） on Hep-2 cell line in vivo and in vitro, in order to explore its possibility in biological treatment of laryngocarcinoma. Methods： Effects of 5-Aza-Cdr and TSA in combination with Ad-p53 on Hep-2 cell line in vivo were determined by Cell Counting Kit-8 （CCK-8） assay. The effect of drug combination was calculated by Jin＇s formula. Effects on the cell line in vitro were investigated by establishing the nude mice model. Results： 5-Aza-Cdr and TSA showed inhibitory effects on the proliferation of Hep-2 cells in dose- and time-dependent manner. Ad-p53 can inhibit the growth of Hep-2 cells in vivo and in vitro. However, the combination of epigenetic reagents （5-Aza-Cdr/TSA） and Ad-p53 was less effective than individual use of Ad-p53. 5-Aza-Cdr and Ad-p53 inhibited the growth of transplanted tumors and reduced the volume of tumors, and the tumor volume of Ad-p53 group was significantly smaller than that of the control group （P0.05）. Conclusion： Both epigenetic reagents （5-Aza-Cdr/TSA） and Ad-p53 can suppress cell proliferation on Hep-2 in vivo and in vitro and there may be some antagonistic mechanism between Ad-p53 and epigenetic reagents （5-Aza-Cdr/ TSA）.
文摘Objective：The aim of this study was to investigate the af ecting of Rg3 to secreted VEGF of human laryngeal carcinoma Hep-2 cells and its mechanism of inhibition to tumor angiogenesis. Methods：Cultured human laryngeal cancer cellline Hep-2 and human vascular endothelial cells in vitro, cells got into the period of exponential phase of growth, was diviced into 3 groups：group I （control group）, group II （DDP group）, group III （Rg3 group）. Added to the Hep-2 cells Rg3 and DDP, made Rg3 final concentration was 300μg/mL, and DDP was 3μg/mL. 48 h later, specimens from sample to be done immunocytochemistry, and the protein of VEGF in Hep-2 cells to be detected. Col ecting Hep-2 cells supernatant, some was used to measure the protein level of VEGF in Hep-2 cells supernatant by ELISA. Some was used to culture HVEC. 24 h later, cellgrowth inhibition rate of human vascular endothelial was determined by MTT. Results：The protein level of VEGF was evi-dently higher in group I compared to group II and group III, it was not only in Hep-2 cells, but also in supernatant of Hep-2 cells. There was no significantly dif erent between group II and group III. MTT results showed that, the human vascular endothelial cellgrowth inhibition rate of group I was significantly lower than that of group II and group III （P〈0.05）. At the same time the HVEC growth inhibition rate of group II was significantly lower than that of group III （P〈0.05）. Conclusion：The inhibition to tumor angiogenesis of Rg3 is stronger than traditional chemotherapy drug cisplatin. It worke by reducing the biological ef ects of secreted VEGF, But the ef ecting worke by reducing the activity of secreted VEGF itself or af ecting endothelial function of VEGF receptor or some other ways to be further studied.
文摘Objective： The aim of the study was to establish models of Hep-2 laryngeal cancer cell line of different oxygen supplying, trying to investigate the impact of normoxia, hypoxia, reoxygenation after hypoxia on apoptosis and expression of proteins HIF-1α and p53 to Hep-2 human laryngeal cancer cell line induced by ^60Co γ-ray. Methods： Human laryngeal cancer Hep-2 cells were divided into 3 groups： group A （normoxia）, group B （hypoxia）, and group C （reoxygenation after hypoxia）. All of the cells were exposed to 5 Gy dosage of γ-ray. Flow cytometry （FCM） was used tomeasure the protein levels of HIF-1α and p53 and to detect cell apoptosis. The protein levels of HIF-la and p53 were also determined by immunohistochemistry and Western blotting. The expression of HIF-la mRNA was determined by RT-PCR. Results： The protein levels of HIF-1α and p53 were evidently increased in group B compared to group A. The protein levels of HIF-1α and p53 in group C were lower compared to group B; the rate of apoptosis in group C was higher than that in group B. Conclusion： Hypoxia decreased the effect of apoptosis induced by ^60Co γ-ray in Hep-2 human laryngeal cancer cell line. The apoptosis pathway maybe related to some other genes or proteins but not p53 in the conditions of hypoxia and reoxygenation after hypoxia.
文摘Objective： The aim of the study was to investigate the impact of 60Co y-ray on apoptosis, cell cycles and the expression of protein hypoxia-inducible factor-1α （HIF-1α） to Hep-2 cell line in the conditions of normoxia and hypoxia. Methods： Hep-2 cell were divided into 2 groups： group A （normoxia） and group B （hypoxia）. All of the ceils were exposed to y-ray with dosage being 0, 1, 3, 5, 10, 20, and 40 Gy. Flow cytometry was used to measure the protein level of HIF-1α and to detect apoptosis and cell cycles. The protein level of HIF-1α was also determined by immunohistochemistry and Western blotting. Results： The protein level of HIF-1α in group B was significantly higher than that in group A. In group A, low doses （1-5 Gy） of y-ray had caused G0/G1 cell cycle arrest and high doses （10-40 Gy） had caused G2/M cell cycle arrest. In group B, without exposure of y-ray （0 Gy） had caused G0/G1 cell cycle arrest, all of the different dosage of y-ray could cause G2/M cell cycle arrest. The curve of apoptosis rate in group A was a parabola, the apoptotic rate was related to the dosage of y-ray in a dosage dependent manner. The peak was at the point of 5 Gy. The apoptosis rate in group A was significantly higher than that in group B. Conclusion： Different doses of y-ray could cause different cell cycles arrest then make different impact on apoptosis to Hep-2 ceil. The lower apoptosis rate in condition of hypoxia maybe has a relationship with G2/M cell cycle arrest. Up-regulated HIF-1α protein may be one of the reasons for G2/M cell cycle arrest.
基金This project was supported by a grant from the Teaching and Research Award Program for Outstanding Young Teacher in Higher Education Institution of Ministry of Education of China.
文摘In order to study the effect of 5, 6-Dichloro-l-13-D-ribofuranosyl-benzimidazole （DRB） on the biological characteristics of human laryngeal carcinoma Hep-2 cell line in vitro, Hep-2 cells cultured in vitro were treated with different concentrations of DRB. Changes in cell proliferation, apoptotic rate and invasiveness were detected by MTT assay, flow cytometry （FCM） and matrigel in vitro invasion assay, respectively. It was found that DRB inhibited the proliferation of Hep-2 cells in a dose- and time-dependent manner. After being treated with 0, 10, 20, 40, 80 μmmol/L DRB for 24 h, the apoptotic rate in Hep-2 cells was （0.68±0.19）%, （1.95±0.12）%, （8.51±0.26）%, （11.26±0.17）% and （14.99±0.32）%, respectively. The matrigel in vitro invasion assay revealed that DRB began to inhibit the invasion of Hep-2 cells at the concentration of 5 μmmol/L, and with the increase of DRB concentration, the inhibitory effect was enhanced. It was suggested that DRB could influence the essential biological characteristics of Hep-2 cells, inhibit Hep-2 cells proliferation, reduce invasive ability and induce apoptosis of Hep-2 cells.
基金This project was supported by the Teaching and Research Award Program for Outstanding Young Teachers in Higher Education Institutions of MOE of China
文摘Summary: The inhibitory effects of two kinds of selective cyclooxygenase-2 inhibitors on the proliferation of human carcinoma of larynx Hep-2 in vitro and their corresponding mechanisms were investigated. Hep-2 cells were cultured with two kinds of selective cyclooxygenase-2 inhibitors (Sc-58125 and Celecoxib) at various concentrations for 24 h. Morphological changes were observed under the phase microscopy and the growth suppression was detected by using MTT colorimetric assay. Apoptotic DNA fragments were observed by agarose gel electrophoresis, and the cell cycle and apoptotic rate were detected by flow cytometry (FCM) respectively. Hep-2 cells became rounded and detached from the culture dish after being treated with Celecoxib for 24 h, however, they remained morphologically unchanged with Sc-58125. Sc-58125 could increase G 2 phase cells, whereas, Celecoxib rose G 1 phase cells. Both of the two effects were dose-dependent. Moreover, the Hep-2 cells cultured with 50 μmol/L and 100 μmol/L Celecoxib showed obvious apoptosis, with the nuclear DNA of cells exhibiting characteristic DNA ladder. So Sc-58125 could inhibit the proliferation of Hep-2 cells by altering the G 2 phase cells. However, Celecoxib had the same effect by changing the G 1 phase cells and inducing apoptosis at higher concentration.
基金ThisstudywassupportedbyShanghaiScienceCommitteeFoundationofChina (No 9844 190 73 )
文摘Objective To develop an improved substrate for indirect immunofluorescence test (IIF) for detecting anti-Ro60/Sjogren's syndrome A (Ro/SSA) autoantibodies.Methods 60-kDa Ro/SSA autoantigens (Ro60) cDNAs were obtained from human placental cDNA library using polymerase chain reaction (PCR) and were cloned into the mammalian expression vector-pEGFP-C1. Then, the recombinant plasmids were transfected into HEp-2 cells. We confirmed the overexpression, localization and antigenicity of fusion proteins in transfected cells by means of immunoblotting, confocal fluorescence microscopy and IIF. HEp-2 and HEp-Ro60 were analyzed by IIF using a panel of 10 precipitin-positive anti-Ro human sera simultaneously.Results Stable expression of Ro60-green fluorescent protein (Ro60-GFP) fusion proteins were maintained ten more generations. Ro60-GFP kept the antigenicity of Ro while demonstrating its own characteristic immunofluorescent pattern in HEp-Ro60 cells. The transfectants dramatically increased the sensitivity of IIF testing (a mean increase of 6.7-fold in endpoint titer). Eight overten (8/10) positive anti-Ro sera showed characteristic immunofluorescent patterns for HEp-Ro60, including two sera that were anti-nuclear antibodies (ANA) negative for untransfected HEp-2. IIF-ANA in all healthy sera was negative for HEp-Ro60. Conclusions As a new substrate for IIF, the Ro60 transfectants can be used to detect anti-Ro antibodies. In addition, transfected HEp-2 cells keep the immunofluorescent properties of HEp-2 cells in IIF-ANA tests and can be employed as a substrate for routine IIF-ANA detection.
文摘Bee venom （BV） was used from long time ago in the medical field as treatment of chronic joint affections. In the recent decades, the screening process of new sources of antimicrobials discovers its high advantageous characteristics for combating various types of microbes, as well as trials to discover its anti-cancer medicinal fields. Lumpy skin disease virus （LSDV） causes disease in cattle of economic importance, and this work aimed to find treatment as well as alternative inactivant for LSDV. The use of bee venom as antiviral was experimented in this work and exhibited satisfied inhibitory effects on LSDV, meanwhile, the antigenic properties was still intact. The viability of virus was tested in tissue culture cells lines and in embryonated chicken eggs. According to doses and time of exposure, the cell lines of Hep-2 （human larynx carcinoma） and MCF7 （breast carcinoma cell line） were treated with different concentrations of BV and examined after 24 h post-inoculation. The Hep-2 and MCF7 cell lines were treated with various concentrations of BV in descending doses as follow： 25, 20, 15, 10, 5 and 0.5 ug/mL of BV. Then bee venom pathological effects on Hep-2 cells and MCF7 cells were observed, such as apoptosis, retarded growths and cytolysis. The results indicate the possibilities of using bee venom as anti-neoplastic and antiviral.
