目的:探讨六棱菊(Laggera alata,L.alata)提取物对乙型肝炎病毒(hepatitis B virus,HBV)感染影响.方法:采用D-氨基半乳糖(D-galactosamine,D-GalN)致人源HL-7702肝细胞损伤模型,研究六棱菊提取物对类似乙型肝炎引起的肝细胞损伤的影响;...目的:探讨六棱菊(Laggera alata,L.alata)提取物对乙型肝炎病毒(hepatitis B virus,HBV)感染影响.方法:采用D-氨基半乳糖(D-galactosamine,D-GalN)致人源HL-7702肝细胞损伤模型,研究六棱菊提取物对类似乙型肝炎引起的肝细胞损伤的影响;采用HBV基因转染的HepG2.2.15细胞模型,评价六棱菊提取物的体外抗HBV作用.通过MTT法检测细胞毒性和细胞活力;通过ELISA和荧光定量PCR法分别检测乙型肝炎表面抗原(hepatitis B virus surface antigen,HBsAg)/乙型肝炎e抗原(hepatitis B e antigen,HBeAg)和HBV DNA水平.结果:六棱菊提取物在25-100μg/mL浓度时,对D-GalN致肝细胞损伤均具有显著保护作用,而在100μg/mL浓度时展示了其最高保护率为45.66%.六棱菊提取物作用HepG2.2.15细胞3d,在10-100μg/mL浓度下对HBsAg有显著抑制作用,其最高抑制率为45.92%;在100μg/mL下能显著抑制HBeAg分泌,其抑制率为50.5%.六棱菊提取物作用HepG2.2.15细胞6 d,在10-100μg/mL浓度下对HBsAg有显著抑制作用,其最高抑制率为84.31%;在25-100μg/mL浓度下能显著抑制HBeAg分泌,最高抑制率为88.45%;同时,在100μg/mL时对HBV DNA复制有显著抑制作用.结论:六棱菊提取物具有较强的体外抗肝细胞损伤作用和抗HBV作用,其抗乙型肝炎作用可能与所含咖啡酰奎宁酸类活性成分有关.展开更多
测定了64株赤芝(Ganoderma lucidum)子实体醇提物清除二苯基苦基苯肼(DPPH)自由基的活性和三萜指纹图谱,采用遗传算法筛选其指纹图谱中的26个共有峰,并标定出其中15个特征峰,运用偏最小二乘回归分析方法(partial least squares regressi...测定了64株赤芝(Ganoderma lucidum)子实体醇提物清除二苯基苦基苯肼(DPPH)自由基的活性和三萜指纹图谱,采用遗传算法筛选其指纹图谱中的26个共有峰,并标定出其中15个特征峰,运用偏最小二乘回归分析方法(partial least squares regression,PLSR)对指纹图谱中26个三萜峰与醇提物清除DPPH自由基的活性进行关联分析,建立了赤芝子实体三萜类化合物的抗氧化谱效关系方程。在赤芝子实体醇提物三萜指纹图谱的26个共有峰中,峰S1、S4、S9、S10和S26的峰面积与醇提物清除DPPH自由基的活性呈显著正相关关系;峰S3、S11、S15、S18、S19、S22和S25的峰面积与醇提物清除DPPH自由基的活性呈显著负相关关系。分别测定鉴定出的15个峰对应的三萜化合物对DPPH自由基的清除活性,发现与清除DPPH自由基活性呈显著正相关的三萜化合物灵芝酸C2(S4)、灵芝酸B(S9)、灵芝酸LM2(S10)、灵芝醛A(S26)对DPPH自由基的清除活性明显高于其他三萜化合物,与清除DPPH自由基活性呈显著负相关的三萜化合物灵芝酮三醇(S18)、灵芝萜酮二醇(S22)无清除DPPH自由基的活性。另外,利用H2O2诱导的PC12细胞损伤模型进一步验证灵芝酸C2、灵芝酸B、灵芝酸LM2、灵芝醛A和灵芝萜酮二醇在细胞水平的抗氧化活性,发现灵芝酸C2、灵芝酸B、灵芝酸LM2、灵芝醛A具有明显的保护神经细胞氧化损伤的活性,而灵芝萜酮二醇对神经细胞的氧化损伤无保护作用。结果表明,本研究建立的赤芝子实体三萜类化合物抗氧化谱效关系方程具有较高的准确性,能够较全面地反应赤芝子实体醇提物中不同三萜化合物与其抗氧化活性的相关性,可快速锁定有效成分以指导活性成分的分离纯化工作。此外,该方法也为赤芝子实体的质量控制提供了更为有效和准确的方法。展开更多
AIM： To study the protective effect of grape procyanidins on oxidative injury induced by ethanol and carbon tetrachloride in rat hepatocytes. METHODS： Normal rat hepatocytes as well as cells damaged by ethanol or ca...AIM： To study the protective effect of grape procyanidins on oxidative injury induced by ethanol and carbon tetrachloride in rat hepatocytes. METHODS： Normal rat hepatocytes as well as cells damaged by ethanol or carbon tetrachloride were incubated with different doses of grape procyanidins for 24 h. Cell proliferation, apoptosis and TNFα mRNA expression were subsequently determined using MTT assay, cell death ELISA and in situ hybridization. RESULTS： Proliferative levels of the control cells from ethanol and CCh injury groups significantly decreased while apoptosis and TNFα mRNA expression significantly increased compared to the normal control and grape procyanidins co-treatment groups （0.455 ± 0.051 vs 0.318 ±0.045, P 〈 0.05）. In comparison with the normal control, 50 and 100 mg/L grape procyanidins significantly stimulated cell growth, with a better effect observed with 100 mg/L grape procyanidins. CONCLUSION： Grape procyanidins inhibit the hepatocyte damage induced by ethanol and carbon tetrachloride, and stimulate normal hepatocyte proliferation.展开更多
Although many previous studies have suggested that estrogen functions as a cytoprotective agent under oxidative stress conditions, the underlying mechanism by which this effect is exerted remains to be elucidated. Thi...Although many previous studies have suggested that estrogen functions as a cytoprotective agent under oxidative stress conditions, the underlying mechanism by which this effect is exerted remains to be elucidated. This study assessed the effects of estradiol-17β （E2） （10^-8s M） on hypoxia-induced cell injury and its related signaling in primary cultured chicken hepatocytes. Hypoxic conditions were found to augment the level of DNA damage and to reduce cell viability and the level of [^3H]-thymidine incorporation, and these phenomena were prevented through treatment with E2. Hypoxia also increased caspase-3 expression, but showed no evidence of an influence on the expression of Bcl-2. However, E2 induced an increase in the level of Bcl-2 expression under hypoxic conditions and reduced the level of caspase-3 expression. The effects of E2 on Bcl-2 and caspase expression were blocked by ICI 182780 （E2 receptor （ER） antagonist, 10＂7 M）. In addition, hypoxia resulted in an increase in the intracellular reactive oxygen species （ROS） generated. These effects were blocked by E2, but not by E2-BSA and ICI 182780. Hypoxia also activated p38 mitogen-activated protein kinase （MAPK）, c-JUN N-terminal kinase/stress-activated protein kinase （JNK/SAPK） and nuclear factor-kB （NF-kB）. These effects were blocked by E2, but not by ICI 182780. The inhibition of p38 MAPK and JNK/SAPK blocked NF-kB activation. In conclusion, E2 was found to protect against hypoxia-induced cell injury in chicken hepatocytes through ER-mediated upregulation of Bcl-2 expression and through reducing the activity of ROS-dependent p38 MAPK, JNK/ SAPK and NF-kB.展开更多
Background Liraglutide is glucagon-like peptide-1 receptor agonist for treating patients with type 2 diabetes mellitus. Our previous studies have demonstrated that liraglutide protects cardiac function through improvi...Background Liraglutide is glucagon-like peptide-1 receptor agonist for treating patients with type 2 diabetes mellitus. Our previous studies have demonstrated that liraglutide protects cardiac function through improving endothelial function in patients with acute myocardial infarction undergoing percutaneous coronary intervention. The present study will investigate whether liraglntide can perform direct protective effects on cardiomyocytes against reperfusion injury. Methods In vitro experiments were performed using H9C2 cells and neonatal rat ventricular cadiomyocytes undergoing simulative hypoxia/reoxygenation （H/R） induction. Cardiomyocytes apoptosis was detected by fluorescence TUNEL. Mitochondrial membrane potential （AWm） and intracellular reactive oxygen species （ROS） was assessed by JC-1 and DHE, respectively. Fura-2/AM was used to measure intracellular Ca2＋ concentration and calcium transient. Immtmofluorescence staining was used to assess the expression level of sarcoplasmic reticulum Ca2＋-ATPase （SERCA2a）. In vivo experiments, myocardial apoptosis and expression of SERCA2a were detected by colorimetric TUNEL and by immunofluorescence staining, respectively. Results In vitro liraglutide inhibited cardiomyotes apoptosis against H/R. △mψ of cardiomyocytes was higher in liraglntide group than H/R group. H/R increased ROS production in H9C2 cells which was attenuated by liraglutide. Liraglutide significantly lowered Ca2＋ overload and improved calcium transient compared with H/R group, lmmunofluorescence staining results showed liraglutide promoted SERCA2a expression which was decreased in H/R group. In ischemia/reperfusion rat hearts, apoptosis was significantly attenuated and SERCA2a expression was increased by liraglutide compared with H/R group. Conclusions Liraglutide can directly protect cardiomyocytes against reperfusion injury which is possibly through modulation of intracellular calcium homeostasis.展开更多
In this experiment, expression of tissue-type plasminogen activator (t-PA) in smooth muscle cells (SMCs) was measured at different intervals after the arterial injury. In the normal iliac arteries, only low levels of ...In this experiment, expression of tissue-type plasminogen activator (t-PA) in smooth muscle cells (SMCs) was measured at different intervals after the arterial injury. In the normal iliac arteries, only low levels of t-PA activity were estimated. t-PA activity in extracts of the iliac arteries increased significantlyat the 4th day after the injury, equivalent to the process that SMCs migrated from the media to the intima,and the t-PA activity was then decreased approximately to the normal level at the 7th day. Coexistent to the above data, results from in situ hybridization showed that the expression of t-PA mRNA in the intima as well as media increased also significantly at the 4th day after the arterial injury, and at the 7th day, tPA mRNA was detected only in those SMCs locating closely adjacent to the internal elastic lamina. These results suggest that t-PA might play an important role in SMC migration following endothelial injury, andantagonism of t-PA expression and/or activity within the vessel wall might be helpful in intervening the de velopment of restenosis following angioplasty.展开更多
Cytophagic histiocytic panniculitis （CHP） was first described by Winkelmann and Bowie in 1980.vj It is a rare group of diverse illnesses involving benign and malignant proliferation of macrophages in various organs ...Cytophagic histiocytic panniculitis （CHP） was first described by Winkelmann and Bowie in 1980.vj It is a rare group of diverse illnesses involving benign and malignant proliferation of macrophages in various organs and tissues. It presents with subcutaneous panniculitis with or without a hemophagocytic syndrome （HPS）. It occurs predominantly in women （male： female ratio 1：1.3） between the years of 5-61 （average, 33.5）. The major clinical features are recurrent fever, multiple panniculitic lesions, anemia, leukopenia and coagulation abnormalities. In the later phase, liver dysfuction, serosal effusion, mucosal ulceration and hemorrhage may occur. Histological findings show activated histiocyte infiltration of the fat tissue. Cytologically the benign-looking histiocytes containing cell fragments （bean-bag cells） are very typical. CHP has a broad spectrum from mild to severe. Benign CHP is selflimiting and sensitive to treatment, but up to now there is no effective therapy for malignant CHP. We report here a case of progressive and fatal cytophagic histiocytic panniculitis in a young woman who had encephaloclastic changes immediately prior to her death.展开更多
Protein Rad23, a nucleotide excision repair factor, mainly involves in repairing the DNA damage from environment, such as UV light. The function of Rad23 protein involved in DNA damage repair from many environmental f...Protein Rad23, a nucleotide excision repair factor, mainly involves in repairing the DNA damage from environment, such as UV light. The function of Rad23 protein involved in DNA damage repair from many environmental factors has been studied extensively, but it is not clear from ultraviolet irradiation. To further investigate the photo-protective function of Rad23 protein on HeLa cells damaged from UV light irradiation, firstly, HeLa cells were irradiated by UV light and incubated with the fusion protein of pCold-Rad23, then the cell viability and apoptosis rate were detected by MTT and Hoechst33342/Pl fluorescent staining, respectively. The results show that the recombinant Rad23 protein can protect the HeLa cells from UV irradiation, and inhibit the apoptosis of HeLa cell by UV irradiation.展开更多
Objective: To investigate the effect of basic fibroblast growth factor (bFGF) and hyaluronic acid (HA) on the proliferation of rabbit chondrocytes in vitro. Methods: Chondrocytes from the knee joints of New Zealand wh...Objective: To investigate the effect of basic fibroblast growth factor (bFGF) and hyaluronic acid (HA) on the proliferation of rabbit chondrocytes in vitro. Methods: Chondrocytes from the knee joints of New Zealand white rabbits were cultured. bFGF or HA or both were added into the culture medium respectively, and the proliferation of the chondrocytes was measured with MTT 3 (4, 5 dimethylthiazol 2 yl) 2, 5 diphenyl tetra zolium bromide. (MTT, Sigma, M2128). Results: Basic fibroblast growth factor (10 ng/ml) with low concentration of fetal bovine serum in the culture medium promoted the proliferation of chondrocytes significantly, and this effect reached its maximum when concentration of bFGF reached 50 ng/ml. HA itself had no effect on the proliferation of chondrocytes. However, when bFGF was used in combination with HA, especially when the concentration of bFGF was 50 500 ng/ml and that of HA was 10 50 ng/ml, the effect on the proliferation of chondrocytes was much more than when bFGF or HA was used alone. Conclusions: bFGF can promote the proliferation of chondrocytes. HA, which has no effect on the proliferation of the cells, can maintain a normal growth of chondrocytes. When bFGF is used in combination with HA, more proliferation is obtained.展开更多
文摘目的:探讨六棱菊(Laggera alata,L.alata)提取物对乙型肝炎病毒(hepatitis B virus,HBV)感染影响.方法:采用D-氨基半乳糖(D-galactosamine,D-GalN)致人源HL-7702肝细胞损伤模型,研究六棱菊提取物对类似乙型肝炎引起的肝细胞损伤的影响;采用HBV基因转染的HepG2.2.15细胞模型,评价六棱菊提取物的体外抗HBV作用.通过MTT法检测细胞毒性和细胞活力;通过ELISA和荧光定量PCR法分别检测乙型肝炎表面抗原(hepatitis B virus surface antigen,HBsAg)/乙型肝炎e抗原(hepatitis B e antigen,HBeAg)和HBV DNA水平.结果:六棱菊提取物在25-100μg/mL浓度时,对D-GalN致肝细胞损伤均具有显著保护作用,而在100μg/mL浓度时展示了其最高保护率为45.66%.六棱菊提取物作用HepG2.2.15细胞3d,在10-100μg/mL浓度下对HBsAg有显著抑制作用,其最高抑制率为45.92%;在100μg/mL下能显著抑制HBeAg分泌,其抑制率为50.5%.六棱菊提取物作用HepG2.2.15细胞6 d,在10-100μg/mL浓度下对HBsAg有显著抑制作用,其最高抑制率为84.31%;在25-100μg/mL浓度下能显著抑制HBeAg分泌,最高抑制率为88.45%;同时,在100μg/mL时对HBV DNA复制有显著抑制作用.结论:六棱菊提取物具有较强的体外抗肝细胞损伤作用和抗HBV作用,其抗乙型肝炎作用可能与所含咖啡酰奎宁酸类活性成分有关.
文摘测定了64株赤芝(Ganoderma lucidum)子实体醇提物清除二苯基苦基苯肼(DPPH)自由基的活性和三萜指纹图谱,采用遗传算法筛选其指纹图谱中的26个共有峰,并标定出其中15个特征峰,运用偏最小二乘回归分析方法(partial least squares regression,PLSR)对指纹图谱中26个三萜峰与醇提物清除DPPH自由基的活性进行关联分析,建立了赤芝子实体三萜类化合物的抗氧化谱效关系方程。在赤芝子实体醇提物三萜指纹图谱的26个共有峰中,峰S1、S4、S9、S10和S26的峰面积与醇提物清除DPPH自由基的活性呈显著正相关关系;峰S3、S11、S15、S18、S19、S22和S25的峰面积与醇提物清除DPPH自由基的活性呈显著负相关关系。分别测定鉴定出的15个峰对应的三萜化合物对DPPH自由基的清除活性,发现与清除DPPH自由基活性呈显著正相关的三萜化合物灵芝酸C2(S4)、灵芝酸B(S9)、灵芝酸LM2(S10)、灵芝醛A(S26)对DPPH自由基的清除活性明显高于其他三萜化合物,与清除DPPH自由基活性呈显著负相关的三萜化合物灵芝酮三醇(S18)、灵芝萜酮二醇(S22)无清除DPPH自由基的活性。另外,利用H2O2诱导的PC12细胞损伤模型进一步验证灵芝酸C2、灵芝酸B、灵芝酸LM2、灵芝醛A和灵芝萜酮二醇在细胞水平的抗氧化活性,发现灵芝酸C2、灵芝酸B、灵芝酸LM2、灵芝醛A具有明显的保护神经细胞氧化损伤的活性,而灵芝萜酮二醇对神经细胞的氧化损伤无保护作用。结果表明,本研究建立的赤芝子实体三萜类化合物抗氧化谱效关系方程具有较高的准确性,能够较全面地反应赤芝子实体醇提物中不同三萜化合物与其抗氧化活性的相关性,可快速锁定有效成分以指导活性成分的分离纯化工作。此外,该方法也为赤芝子实体的质量控制提供了更为有效和准确的方法。
文摘AIM： To study the protective effect of grape procyanidins on oxidative injury induced by ethanol and carbon tetrachloride in rat hepatocytes. METHODS： Normal rat hepatocytes as well as cells damaged by ethanol or carbon tetrachloride were incubated with different doses of grape procyanidins for 24 h. Cell proliferation, apoptosis and TNFα mRNA expression were subsequently determined using MTT assay, cell death ELISA and in situ hybridization. RESULTS： Proliferative levels of the control cells from ethanol and CCh injury groups significantly decreased while apoptosis and TNFα mRNA expression significantly increased compared to the normal control and grape procyanidins co-treatment groups （0.455 ± 0.051 vs 0.318 ±0.045, P 〈 0.05）. In comparison with the normal control, 50 and 100 mg/L grape procyanidins significantly stimulated cell growth, with a better effect observed with 100 mg/L grape procyanidins. CONCLUSION： Grape procyanidins inhibit the hepatocyte damage induced by ethanol and carbon tetrachloride, and stimulate normal hepatocyte proliferation.
文摘Although many previous studies have suggested that estrogen functions as a cytoprotective agent under oxidative stress conditions, the underlying mechanism by which this effect is exerted remains to be elucidated. This study assessed the effects of estradiol-17β （E2） （10^-8s M） on hypoxia-induced cell injury and its related signaling in primary cultured chicken hepatocytes. Hypoxic conditions were found to augment the level of DNA damage and to reduce cell viability and the level of [^3H]-thymidine incorporation, and these phenomena were prevented through treatment with E2. Hypoxia also increased caspase-3 expression, but showed no evidence of an influence on the expression of Bcl-2. However, E2 induced an increase in the level of Bcl-2 expression under hypoxic conditions and reduced the level of caspase-3 expression. The effects of E2 on Bcl-2 and caspase expression were blocked by ICI 182780 （E2 receptor （ER） antagonist, 10＂7 M）. In addition, hypoxia resulted in an increase in the intracellular reactive oxygen species （ROS） generated. These effects were blocked by E2, but not by E2-BSA and ICI 182780. Hypoxia also activated p38 mitogen-activated protein kinase （MAPK）, c-JUN N-terminal kinase/stress-activated protein kinase （JNK/SAPK） and nuclear factor-kB （NF-kB）. These effects were blocked by E2, but not by ICI 182780. The inhibition of p38 MAPK and JNK/SAPK blocked NF-kB activation. In conclusion, E2 was found to protect against hypoxia-induced cell injury in chicken hepatocytes through ER-mediated upregulation of Bcl-2 expression and through reducing the activity of ROS-dependent p38 MAPK, JNK/ SAPK and NF-kB.
基金This work is supported by grants from National Natural Science Foundation of China （No. 81102079） and China Postdoctoral Science Foundation （No. 201003776）. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The authors report no conflict of interest. The authors are responsible for the content and writing of the paper.
文摘Background Liraglutide is glucagon-like peptide-1 receptor agonist for treating patients with type 2 diabetes mellitus. Our previous studies have demonstrated that liraglutide protects cardiac function through improving endothelial function in patients with acute myocardial infarction undergoing percutaneous coronary intervention. The present study will investigate whether liraglntide can perform direct protective effects on cardiomyocytes against reperfusion injury. Methods In vitro experiments were performed using H9C2 cells and neonatal rat ventricular cadiomyocytes undergoing simulative hypoxia/reoxygenation （H/R） induction. Cardiomyocytes apoptosis was detected by fluorescence TUNEL. Mitochondrial membrane potential （AWm） and intracellular reactive oxygen species （ROS） was assessed by JC-1 and DHE, respectively. Fura-2/AM was used to measure intracellular Ca2＋ concentration and calcium transient. Immtmofluorescence staining was used to assess the expression level of sarcoplasmic reticulum Ca2＋-ATPase （SERCA2a）. In vivo experiments, myocardial apoptosis and expression of SERCA2a were detected by colorimetric TUNEL and by immunofluorescence staining, respectively. Results In vitro liraglutide inhibited cardiomyotes apoptosis against H/R. △mψ of cardiomyocytes was higher in liraglntide group than H/R group. H/R increased ROS production in H9C2 cells which was attenuated by liraglutide. Liraglutide significantly lowered Ca2＋ overload and improved calcium transient compared with H/R group, lmmunofluorescence staining results showed liraglutide promoted SERCA2a expression which was decreased in H/R group. In ischemia/reperfusion rat hearts, apoptosis was significantly attenuated and SERCA2a expression was increased by liraglutide compared with H/R group. Conclusions Liraglutide can directly protect cardiomyocytes against reperfusion injury which is possibly through modulation of intracellular calcium homeostasis.
文摘In this experiment, expression of tissue-type plasminogen activator (t-PA) in smooth muscle cells (SMCs) was measured at different intervals after the arterial injury. In the normal iliac arteries, only low levels of t-PA activity were estimated. t-PA activity in extracts of the iliac arteries increased significantlyat the 4th day after the injury, equivalent to the process that SMCs migrated from the media to the intima,and the t-PA activity was then decreased approximately to the normal level at the 7th day. Coexistent to the above data, results from in situ hybridization showed that the expression of t-PA mRNA in the intima as well as media increased also significantly at the 4th day after the arterial injury, and at the 7th day, tPA mRNA was detected only in those SMCs locating closely adjacent to the internal elastic lamina. These results suggest that t-PA might play an important role in SMC migration following endothelial injury, andantagonism of t-PA expression and/or activity within the vessel wall might be helpful in intervening the de velopment of restenosis following angioplasty.
文摘Cytophagic histiocytic panniculitis （CHP） was first described by Winkelmann and Bowie in 1980.vj It is a rare group of diverse illnesses involving benign and malignant proliferation of macrophages in various organs and tissues. It presents with subcutaneous panniculitis with or without a hemophagocytic syndrome （HPS）. It occurs predominantly in women （male： female ratio 1：1.3） between the years of 5-61 （average, 33.5）. The major clinical features are recurrent fever, multiple panniculitic lesions, anemia, leukopenia and coagulation abnormalities. In the later phase, liver dysfuction, serosal effusion, mucosal ulceration and hemorrhage may occur. Histological findings show activated histiocyte infiltration of the fat tissue. Cytologically the benign-looking histiocytes containing cell fragments （bean-bag cells） are very typical. CHP has a broad spectrum from mild to severe. Benign CHP is selflimiting and sensitive to treatment, but up to now there is no effective therapy for malignant CHP. We report here a case of progressive and fatal cytophagic histiocytic panniculitis in a young woman who had encephaloclastic changes immediately prior to her death.
基金Project(31171176)supported by the National Natural Science Foundation of China
文摘Protein Rad23, a nucleotide excision repair factor, mainly involves in repairing the DNA damage from environment, such as UV light. The function of Rad23 protein involved in DNA damage repair from many environmental factors has been studied extensively, but it is not clear from ultraviolet irradiation. To further investigate the photo-protective function of Rad23 protein on HeLa cells damaged from UV light irradiation, firstly, HeLa cells were irradiated by UV light and incubated with the fusion protein of pCold-Rad23, then the cell viability and apoptosis rate were detected by MTT and Hoechst33342/Pl fluorescent staining, respectively. The results show that the recombinant Rad23 protein can protect the HeLa cells from UV irradiation, and inhibit the apoptosis of HeLa cell by UV irradiation.
文摘Objective: To investigate the effect of basic fibroblast growth factor (bFGF) and hyaluronic acid (HA) on the proliferation of rabbit chondrocytes in vitro. Methods: Chondrocytes from the knee joints of New Zealand white rabbits were cultured. bFGF or HA or both were added into the culture medium respectively, and the proliferation of the chondrocytes was measured with MTT 3 (4, 5 dimethylthiazol 2 yl) 2, 5 diphenyl tetra zolium bromide. (MTT, Sigma, M2128). Results: Basic fibroblast growth factor (10 ng/ml) with low concentration of fetal bovine serum in the culture medium promoted the proliferation of chondrocytes significantly, and this effect reached its maximum when concentration of bFGF reached 50 ng/ml. HA itself had no effect on the proliferation of chondrocytes. However, when bFGF was used in combination with HA, especially when the concentration of bFGF was 50 500 ng/ml and that of HA was 10 50 ng/ml, the effect on the proliferation of chondrocytes was much more than when bFGF or HA was used alone. Conclusions: bFGF can promote the proliferation of chondrocytes. HA, which has no effect on the proliferation of the cells, can maintain a normal growth of chondrocytes. When bFGF is used in combination with HA, more proliferation is obtained.
