Objective To explore the change of gene expression of stress activated protein kinase (SAPK) and its upstream signalregulated molecule ——mitogen activated protein kinases(MAPKs) (MKK4 and MKK7) in hypertrophic scar and autocontrol normal skin. Methods The total RNA was isolated from 8 hypertrophic scars and 8 auto-control skin, and then mRNA was purified. The gene expressions of MKK4, MKK7 and SAPK were examined with reverse transcriptionpolymerase chain reaction(RT-PCR) method. Results In hypertrophic scar, both MKK7 and SAPK genes weakly expressed. In auto-control skin, the expression of these 2 genes was significantly elevated in comparison with hypertrophic scar (Plt;0.01). The expression levelsof these 2 genes were 1.5 times and 2.6 times as long as those of hypertrophic scar, respectively. Gene expression of MKK4 had no significant difference between autocontrol skin and hypertrophic scar (Pgt;0.05). Conclusion Decreased gene expression of MKK7 and SAPK which results in reducing cell apoptosis might be one of the mechanisms for controlling the formation of hypertrophic scar.
Objective To observe the effects of epidural anaesthesia (EA) and general anaesthesia (GA) on the changes of plasma epinephrine (E) and norepinephrine (NE) during laparoscopic cholecystectomy (LC). Methods Thirty patients undergoing elective LC were randomly divided into GA group (n=15) and EA group (n=15). The concentrations of plasma NE and E were measured at the following phases: before anaesthesia, before introducing pneumoperitoneum, during pneumoperitoneum, and at the end of operation. Results In EA group, the concentrations of NE weren′t significantly different at each phase, the concentrations of E significantly increased before and during pneumoperitoneum (P<0.05) and returned to the baseline at the end of operation (P>0.05). In GA group, the concentrations of NE and E didn′t change significantly before pneumoperitoneum, but increased during pneumoperitoneum (P<0.05) and E didn′t return to the baseline at the end of operation (P<0.05). The E concentrations of EA group was higher than that of GA group before pneumoperitoneum, but the NE concentration of EA group was lower than that of GA group during pneumoperitoneum (P<0.05). Conclusion Both groups has significant stress reaction, but the stress reaction of EA group is weaker than that of GA group during LC.
摘要:目的:通过建立高脂血症脂肪肝动物模型,探讨杜仲叶醇提取物(alcohol extractive of Folium Eucommiae,AEFE)对脂肪肝的防治作用。方法:高脂饮食8周加维生素D36×105IU/kg分3d腹腔注射,建立大鼠高脂血症脂肪肝动物模型。各给药组从造模第3周开始分别灌胃给予洛伐他汀(4mg·kg-1·d-1)、 AEFE(70、140和420mg·kg-1·d-1),共给药6周。各组每天灌服等量生理盐水,灌胃容积为0.5mL/100g体重。结果:AEFE用药6周后显示,各剂量组血清胆固醇、甘油三酯和游离脂肪酸、谷丙转氨酶和谷草转氨酶均较模型组明显降低(Plt;005),肝组织丙二醛含量降低和超氧化物歧化酶活性升高,肝脂肪变性和炎症反应减轻,尤以中剂量组作用最明显(Plt;001)。AEFE对肝内肿瘤坏死因子α浓度无明显影响。结论:AEFE改善高脂性大鼠肝脏脂肪变性,此作用可能与其降血脂、抗氧化损伤有关。
ObjectiveTo identify causal effects and potential mechanisms of oxidative stress (OS) genes in lung cancer. MethodsOS-related genes were extracted from the GeneCards database. Integration analysis of genome-wide association study (GWAS) data for lung cancer with gene expression and DNA methylation quantitative trait loci (eQTL and mQTL) in blood was performed using the summary data-based Mendelian randomization (SMR) approach to determine the causal relationship between OS genes and lung cancer risk. Colocalization analysis of OS gene QTLs and lung cancer risk loci was performed to gain insight into the potential regulatory mechanisms of lung cancer risk. ResultsA potential causal relationship between OS-related genes and lung cancer was identified by SMR analysis. AGER expression level was found to be associated with lung cancer risk [OR=1.944, 95%CI (1.431, 2.640), P<0.001], and ATF6B expression level was associated with lung cancer risk [OR=1.508, 95%CI (1.287, 1.767), P<0.001]. Meanwhile, ATF6B methylation level was associated with lung cancer risk. ConclusionOS-related genes are associated with lung cancer, which may be a potential site of action for anti-cancer drugs.
Metabolic memory means if the hyperglycemia can't be controlled at early stage of diabetes, chronic complications such as diabetic retinopathy (DR) will continue to develop even if the blood glucose level maintains normal level at later stage. Oxidative stress plays an important role in the "metabolic memory" of DR, which interacts with the nitrative stress, advanced glycation end products, genetic modification and endoplasmic reticulum stress in the pathogenesis of DR. Further elucidation of the relationship between oxidative stress and "metabolic memory" of DR can open the way for the discovery of novel therapeutic targets to prevent DR progression.
ObjectiveTo investigate the effects of phenethyl isothiocyanate (PEITC) on apoptosis and proliferation of breast cancer SK-BR-3 cells. MethodsSK-BR-3 cells were treated with different concentrations (0, 10, 30, 50 μmol/L) of PEITC respectively. The proliferation capacity of SK-BR-3 cells was detected by MTT and BrdU staining methods. The cell apoptosis was detected by TUNEL and flow cytometry methods. The protein and mRNA expressions levels of indexes related apoptosis such as Bcl-2, Bax, and MCL-1 and indexes related endoplasmic reticulum stress (ERS) such as PERK, eIF2α, CHOP, IRE1α, ATF6α were detected by Western blot and quantitative real-time PCR (qRT-PCR), respectively. ResultsCompared with the control group (0 μmol/L PEITC treatment group), the results of MTT and BrdU staining methods showed that the proliferations of SK-BR-3 cells in the 10, 30 and 50 μmol/L PEITC treatment group were decreased in turn with the increase of concentration. The results of TUNEL and flow cytometry methods showed that the apoptosis rates of SK-BR-3 cells in the 10, 30 and 50 μmol/L PEITC treatment group were increased in turn with the increase of concentration. The results of Western blot and qRT-PCR methods showed that the protein and mRNA expression levels of anti-apoptotic indexes (Bcl-2, MCL-1) were decreased with the increase of concentration, while the expression levels of protein and mRNA of the pro-apoptotic index (Bax) and ERS-related indexes (PERK, eIF2α, CHOP, IRE1α, ATF6α) increased with the increase of concentration. ConclusionFrom the preliminary results of this study, PEITC can promote the apoptosis of breast cancer SK-BR-3 cells and inhibit cell proliferation, which might be achieved by regulating the expression levels of indexes related apoptosis and ERS.
Age-related macular degeneration (AMD) is one of the leading irreversible causes of blindness in China. The pathogenesis of AMD is not fully understood at present. Under various stress conditions, cellular senescence is activated, characterized by telomere shortening, mitochondrial dysfunction, DNA damage, and the release of various senescence-related secretory phenotype factors. Senescence is implicated in the pathogenesis of AMD through multiple pathways, contributing to chronic inflammation and the onset and progression of AMD. Mechanisms such as oxidative stress, lipofuscin, β amyloid protein and the membrane attack complex have become hotspots of study in the pathogenesis of AMD. The cyclic guanosine phosphate - adenosine synthase - interferon stimulating factor synthase-stimulator of interferon gene pathway has emerged as a critical signaling pathway in the early development of AMD, providing direction for further research on AMD. Currently, senolytics, selective agents targeting the induction of senescent cell apoptosis, show significant potential in the treatment of AMD. The integration of new technologies with cellular senescence may offer a novel approach to AMD treatment, and intervening in the AMD treatment through anti-cellular senescence pathways holds promising prospects.