Background:Although the buried wood of Phoebe zhennan is known as the“mummy”of the plant kingdom,there is little research on its pharmacological activity.This study endeavored to investigate the effect and mechanism...Background:Although the buried wood of Phoebe zhennan is known as the“mummy”of the plant kingdom,there is little research on its pharmacological activity.This study endeavored to investigate the effect and mechanism of buried wood of Phoebe zhennan extract(BPE)on physical fatigue mice induced by weight-loaded forced swimming.Methods:Firstly,BPE was obtained by 70%ethanol extraction and freeze-drying processes.Then,the effect of BPE on physical fatigue mice was evaluated by swimming time,rotating stick time,levels of lipid peroxidation,lactate,lactate dehydrogenase,urea nitrogen,creatine kinase and muscle glycogen.Finally,real time fluorescence quantification and western blot were used to investigate the possible mechanism of BPE.Results:BPE could significantly alleviate muscle tissue damage,prolong the exhaustion time of weight-bearing swimming and rotating stick time.Meanwhile,BPE treatment could notably reduce the accumulation of serum lactate,urea nitrogen,and activities of lactate dehydrogenase and creatine kinase,while increasing the levels of glycogen and activities of glutathione peroxidase and superoxide dismutase in muscles.Moreover,BPE treatment obviously increased HO-1,Nrf-2,AMPK,PGC-1αmRNA and protein expressions in the muscles of physical fatigue mice.Conclusion:BPE treatment could ameliorate various impairments and oxidative stress injury induced by physical fatigue via activating Nrf-2/HO-1 and AMPK/PGC-1αsignaling pathway.展开更多
目的:研究活化蛋白C(Activated protein C,APC)对大鼠皮瓣缺血再灌注损伤的作用及可能机制。方法:将80只SD雄性大鼠随机分为四组:对照组、药物对照组、模型组和治疗组,每组20只。观察术后72 h内模型大鼠皮瓣形态变化,HE染色观察大鼠皮...目的:研究活化蛋白C(Activated protein C,APC)对大鼠皮瓣缺血再灌注损伤的作用及可能机制。方法:将80只SD雄性大鼠随机分为四组:对照组、药物对照组、模型组和治疗组,每组20只。观察术后72 h内模型大鼠皮瓣形态变化,HE染色观察大鼠皮瓣组织病理学变化,TUNEL法染色观察皮瓣组织细胞凋亡,ELISA法检测血清中TNF-α、IL-6水平,用黄嘌呤氧化酶法和硫代巴比妥酸TBA比色法分别测定皮瓣组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量,Westernblot法检测皮瓣组织中Nrf-2、HO-1、γ-GCS蛋白表达水平。结果:与模型组比较,治疗组皮瓣红肿、坏死程度、病理损伤程度减弱;TUNEL法染色观察,与模型组比较,治疗组皮瓣组织细胞凋亡率减少(P<0.05);ELISA法检测发现,与模型组比较,治疗组血清中TNF-α、IL-6降低(P<0.05);与模型组比较,治疗组SOD活性升高(P<0.05),MDA含量降低(P<0.05);Westernblot法检测发现,与模型组比较,治疗组Nrf-2、HO-1、γ-GCS蛋白相对表达水平上升(P<0.05)。结论:APC能改善大鼠皮瓣缺血再灌注损伤,其机制可能与激活Nrf-2/HO-1信号通路,抑制氧化应激反应和减少细胞凋亡、炎症反应有关。展开更多
We investigated the liver protective activity of dandelion polyphenols(DP)against acetaminophen(APAP;Paracetamol)-induced hepatotoxicity.Mice were acclimated for 1 week and randomly divided into the following groups(n...We investigated the liver protective activity of dandelion polyphenols(DP)against acetaminophen(APAP;Paracetamol)-induced hepatotoxicity.Mice were acclimated for 1 week and randomly divided into the following groups(n=9 per group):Control,APAP,APAP+DP(100 mg·kg^–1),APAP+DP(200 mg·kg^–1),and APAP+DP(400 mg·kg^–1)groups.Mice were pretreated with DP(100,200,and 400 mg·kg^–1)by oral gavage for 7 d before being treated with 350 mg·kg^–1 APAP for 24 h to induced hepatotoxicity.Severe liver injury was observed,and hepatotoxicity was analyzed after 24 h by evaluation of biochemical markers,protein expressions levels,and liver histopathology.Pretreatment with DP was able to restore serum liver characteristics(aspartate transaminase,AST;alanine aminotransferase,ALT;alkaline phosphatase,AKP),improve redox imbalance(superoxide dismutase,SOD;glutathione,GSH;malondialdehyde,MDA),and decrease inflammatory factors(tumor necrosis factor-α,TNF-α;interleukin-1β,IL-1β).Pretreatment with DP also significantly inhibited the expression levels of nitric oxide synthase(iNOS)and cyclooxygenase-2(COX-2).Furthermore,DP pretreatment could inhibit the apoptosis of liver cells caused by APAP through up-regulation of Bcl-2 and down-regulation of Bax and caspase-9 protein.DP also down-regulated p-JNK protein expression levels to inhibit APAP-induced mitochondrial oxidative stress and up-regulated the expression of Nrf-2 and its target gene HO-1.The histopathological staining demonstrated that DP pretreatment could inhibit APAP-induced hepatocyte infiltration,congestion,and necrosis.Our results demonstrate that DP pretreatment could protect against APAP-induced hepatic injury by activating the Nrf-2/HO-1 pathway and inhibition of the intrinsic apoptosis pathway.展开更多
基金supported by the Scientific Research Foundation for the introduction of talent of Pingdingshan University(No.PXY-BSQD-2022040,PXY-BSQD-2023024)Henan Province Science and Technology Research Project(No.242102310313,232102310460).
文摘Background:Although the buried wood of Phoebe zhennan is known as the“mummy”of the plant kingdom,there is little research on its pharmacological activity.This study endeavored to investigate the effect and mechanism of buried wood of Phoebe zhennan extract(BPE)on physical fatigue mice induced by weight-loaded forced swimming.Methods:Firstly,BPE was obtained by 70%ethanol extraction and freeze-drying processes.Then,the effect of BPE on physical fatigue mice was evaluated by swimming time,rotating stick time,levels of lipid peroxidation,lactate,lactate dehydrogenase,urea nitrogen,creatine kinase and muscle glycogen.Finally,real time fluorescence quantification and western blot were used to investigate the possible mechanism of BPE.Results:BPE could significantly alleviate muscle tissue damage,prolong the exhaustion time of weight-bearing swimming and rotating stick time.Meanwhile,BPE treatment could notably reduce the accumulation of serum lactate,urea nitrogen,and activities of lactate dehydrogenase and creatine kinase,while increasing the levels of glycogen and activities of glutathione peroxidase and superoxide dismutase in muscles.Moreover,BPE treatment obviously increased HO-1,Nrf-2,AMPK,PGC-1αmRNA and protein expressions in the muscles of physical fatigue mice.Conclusion:BPE treatment could ameliorate various impairments and oxidative stress injury induced by physical fatigue via activating Nrf-2/HO-1 and AMPK/PGC-1αsignaling pathway.
文摘目的:研究活化蛋白C(Activated protein C,APC)对大鼠皮瓣缺血再灌注损伤的作用及可能机制。方法:将80只SD雄性大鼠随机分为四组:对照组、药物对照组、模型组和治疗组,每组20只。观察术后72 h内模型大鼠皮瓣形态变化,HE染色观察大鼠皮瓣组织病理学变化,TUNEL法染色观察皮瓣组织细胞凋亡,ELISA法检测血清中TNF-α、IL-6水平,用黄嘌呤氧化酶法和硫代巴比妥酸TBA比色法分别测定皮瓣组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量,Westernblot法检测皮瓣组织中Nrf-2、HO-1、γ-GCS蛋白表达水平。结果:与模型组比较,治疗组皮瓣红肿、坏死程度、病理损伤程度减弱;TUNEL法染色观察,与模型组比较,治疗组皮瓣组织细胞凋亡率减少(P<0.05);ELISA法检测发现,与模型组比较,治疗组血清中TNF-α、IL-6降低(P<0.05);与模型组比较,治疗组SOD活性升高(P<0.05),MDA含量降低(P<0.05);Westernblot法检测发现,与模型组比较,治疗组Nrf-2、HO-1、γ-GCS蛋白相对表达水平上升(P<0.05)。结论:APC能改善大鼠皮瓣缺血再灌注损伤,其机制可能与激活Nrf-2/HO-1信号通路,抑制氧化应激反应和减少细胞凋亡、炎症反应有关。
基金supported by the National Natural Science Foundation of China(Nos.81202935 and 81773893)the National Major Scientific and Technological Special Project of China for “Significant New Drugs Development”(No.2017ZX09301060-001)+1 种基金the Natural Science Foundation of Hubei Province,China(No.2015CFB302)Fundamental Research Funds for the Central Universities “South-Central University for Nationalities”(No.CZY20025)。
文摘We investigated the liver protective activity of dandelion polyphenols(DP)against acetaminophen(APAP;Paracetamol)-induced hepatotoxicity.Mice were acclimated for 1 week and randomly divided into the following groups(n=9 per group):Control,APAP,APAP+DP(100 mg·kg^–1),APAP+DP(200 mg·kg^–1),and APAP+DP(400 mg·kg^–1)groups.Mice were pretreated with DP(100,200,and 400 mg·kg^–1)by oral gavage for 7 d before being treated with 350 mg·kg^–1 APAP for 24 h to induced hepatotoxicity.Severe liver injury was observed,and hepatotoxicity was analyzed after 24 h by evaluation of biochemical markers,protein expressions levels,and liver histopathology.Pretreatment with DP was able to restore serum liver characteristics(aspartate transaminase,AST;alanine aminotransferase,ALT;alkaline phosphatase,AKP),improve redox imbalance(superoxide dismutase,SOD;glutathione,GSH;malondialdehyde,MDA),and decrease inflammatory factors(tumor necrosis factor-α,TNF-α;interleukin-1β,IL-1β).Pretreatment with DP also significantly inhibited the expression levels of nitric oxide synthase(iNOS)and cyclooxygenase-2(COX-2).Furthermore,DP pretreatment could inhibit the apoptosis of liver cells caused by APAP through up-regulation of Bcl-2 and down-regulation of Bax and caspase-9 protein.DP also down-regulated p-JNK protein expression levels to inhibit APAP-induced mitochondrial oxidative stress and up-regulated the expression of Nrf-2 and its target gene HO-1.The histopathological staining demonstrated that DP pretreatment could inhibit APAP-induced hepatocyte infiltration,congestion,and necrosis.Our results demonstrate that DP pretreatment could protect against APAP-induced hepatic injury by activating the Nrf-2/HO-1 pathway and inhibition of the intrinsic apoptosis pathway.
