目的 探究A型肉毒毒素(botulinum toxin type-A, BTX-A)对紫外线诱导光老化大鼠皮肤损伤的影响及其作用机制。方法 自2020年7月至2021年2月,河北工程大学附属医院将40只大鼠分为正常组、模型组、1.5 U BTX-A组、3.0 U BTX-A组、6.0 U BT...目的 探究A型肉毒毒素(botulinum toxin type-A, BTX-A)对紫外线诱导光老化大鼠皮肤损伤的影响及其作用机制。方法 自2020年7月至2021年2月,河北工程大学附属医院将40只大鼠分为正常组、模型组、1.5 U BTX-A组、3.0 U BTX-A组、6.0 U BTX-A组。观察HE染色、Masson染色观察组织形态,SA-β-Gal半乳糖染色观察细胞衰老,TUNEL染色检测细胞凋亡;试剂盒检测皮肤组织中超氧化物歧化酶(superoxide dismutase, SOD)、羟脯氨酸(hydroxyproline, HYP)、丙二醛(malondialdehyde, MDA)水平;蛋白质免疫印迹法检测皮肤组织中老化标志物(细胞周期调控因子p16、p21、p53)、细胞凋亡相关蛋白(抗凋亡bcl-2蛋白、促凋亡bax蛋白)、高迁移率族蛋白B1(high mobility group protein B1, HMGB1)、晚期糖基化终产物受体(receptor of advanced glycation end products, RAGE)、核因子κB亚基p65(NF-κB p65)表达水平。结果 正常组表皮结构完整,胶原纤维排列致密;模型组表皮增厚,出现炎性细胞浸润,胶原纤维排列疏松;1.5、3.0、6.0 U BTX-A组较模型组有所改善,表皮少量增厚,胶原纤维排列分散程度变小。相较于正常组,模型组和BTX-A各剂量组p16、p21、p53、HMGB1、RAGE、NF-κB p65表达以及MDA含量均显著升高,Bcl-2/Bax水平以及SOD、HYP活性显著降低(P<0.05);相较于模型组,1.5、3.0、6.0 U BTX-A组p16、p21、p53、HMGB1、RAGE、NF-κB p65表达以及MDA含量显著降低,Bcl-2/Bax水平以及SOD、HYP活性显著升高(P<0.05)。结论 BTX-A对紫外线诱导光老化大鼠皮肤损伤具有保护作用,可能是通过HMGB1/RAGE通路发挥作用的。展开更多
In the present study, the involvement of L-arginine(L-Arg) NO on the protective action of electroacupuncture(EA) on cerebral ischemic injury was observed in acute ischemia-reperfusion(IR) rat model by taking regional ...In the present study, the involvement of L-arginine(L-Arg) NO on the protective action of electroacupuncture(EA) on cerebral ischemic injury was observed in acute ischemia-reperfusion(IR) rat model by taking regional cerebral blood flow(r-CBF),cerebral water content(CWC),and blood nitric oxide(NO) contents as indexes. Results showed that 1) EA could cause r-CBF and serum NO content to increase and CWC to lower, suggesting an protective action of EA on IR cerebral injury; 2) intravenous injection of L-Arg also had an protective effect on cerebral IR cerebral injury, while L-NNA had no this effect; and 3) pre-treatment with L-Arg might strengthen the effect of EA further, while pretreatment with L-NNA could weaken its effect. It indicates that L-Arg-NO may be involved in the effect of EA in protecting the brain from ischemic injury.展开更多
文摘目的 探究A型肉毒毒素(botulinum toxin type-A, BTX-A)对紫外线诱导光老化大鼠皮肤损伤的影响及其作用机制。方法 自2020年7月至2021年2月,河北工程大学附属医院将40只大鼠分为正常组、模型组、1.5 U BTX-A组、3.0 U BTX-A组、6.0 U BTX-A组。观察HE染色、Masson染色观察组织形态,SA-β-Gal半乳糖染色观察细胞衰老,TUNEL染色检测细胞凋亡;试剂盒检测皮肤组织中超氧化物歧化酶(superoxide dismutase, SOD)、羟脯氨酸(hydroxyproline, HYP)、丙二醛(malondialdehyde, MDA)水平;蛋白质免疫印迹法检测皮肤组织中老化标志物(细胞周期调控因子p16、p21、p53)、细胞凋亡相关蛋白(抗凋亡bcl-2蛋白、促凋亡bax蛋白)、高迁移率族蛋白B1(high mobility group protein B1, HMGB1)、晚期糖基化终产物受体(receptor of advanced glycation end products, RAGE)、核因子κB亚基p65(NF-κB p65)表达水平。结果 正常组表皮结构完整,胶原纤维排列致密;模型组表皮增厚,出现炎性细胞浸润,胶原纤维排列疏松;1.5、3.0、6.0 U BTX-A组较模型组有所改善,表皮少量增厚,胶原纤维排列分散程度变小。相较于正常组,模型组和BTX-A各剂量组p16、p21、p53、HMGB1、RAGE、NF-κB p65表达以及MDA含量均显著升高,Bcl-2/Bax水平以及SOD、HYP活性显著降低(P<0.05);相较于模型组,1.5、3.0、6.0 U BTX-A组p16、p21、p53、HMGB1、RAGE、NF-κB p65表达以及MDA含量显著降低,Bcl-2/Bax水平以及SOD、HYP活性显著升高(P<0.05)。结论 BTX-A对紫外线诱导光老化大鼠皮肤损伤具有保护作用,可能是通过HMGB1/RAGE通路发挥作用的。
文摘In the present study, the involvement of L-arginine(L-Arg) NO on the protective action of electroacupuncture(EA) on cerebral ischemic injury was observed in acute ischemia-reperfusion(IR) rat model by taking regional cerebral blood flow(r-CBF),cerebral water content(CWC),and blood nitric oxide(NO) contents as indexes. Results showed that 1) EA could cause r-CBF and serum NO content to increase and CWC to lower, suggesting an protective action of EA on IR cerebral injury; 2) intravenous injection of L-Arg also had an protective effect on cerebral IR cerebral injury, while L-NNA had no this effect; and 3) pre-treatment with L-Arg might strengthen the effect of EA further, while pretreatment with L-NNA could weaken its effect. It indicates that L-Arg-NO may be involved in the effect of EA in protecting the brain from ischemic injury.
