Objective:To investigate the mechanism of electroacupuncture (EA) at "Zusanli" (ST36) and "Taichong" (LR3) for attenuating duodenal injury in rats with functional dyspepsia (FD) based on ferroptosis mediated by Kelch-like epichlorohydrin-associated protein 1 (Keap1)/nuclear factor E2-related factor 2 (Nrf2)/glutathione peroxidase 4 (GPX4) pathway. Methods:A total of 21 SPF-grade SD male rats were randomly divided into a normal group, a model group and an EA group, 7 rats in each one. In the model and EA groups, FD (liver stagnation and spleen deficiency) models were prepared by dual-factor combination method, using mild tail clamping stimulation and intermittent diet. After model preparation, in the EA group, EA was operated at bilateral "Zusanli" (ST36) and "Taichong" (LR3), with a disperse-dense wave, a frequency of 2 Hz/100 Hz and for 20 min each session, once a day, and the duration of intervention was composed of 14 days. The general condition of the rats was observed. The gastric emptying rate and intestinal propulsion rate were measured. The pathomorphologic changes of duodenal tissue were observed by HE staining method; the positive expression of Keap1, Nrf2 and GPX4 in duodenal tissue was detected using immunohistochemistry and the positive expression of reactive oxygen species (ROS) in duodenal tissue was detected using immunofluorescence. The levels of ferrous ions (Fe2+) in duodenal tissue, and malondialdehyde (MDA), reduced glutathione (GSH) and superoxide dismutase (SOD) in serum were detected using biochemical methods, ATP level in serum was detected using ELISA, and the mRNA expression of Keap1, Nrf2, and GPX4 in duodenal tissue was detected by real-time fluorescence quantitative PCR (RT-qPCR); and the protein expression of Keap1, Nrf2, GPX4, acyl-CoA synthase long-chain family 4 (ACSL4) and solute carrier family 7 member 11 (SLC7A11) was detected using Western blot. Results:Compared with the normal group, the rats in the model group exhibited the decrease in food intake, body weight, gastric emptying rate and intestinal propulsion rate (P<0.05). In the duodenal tissue, the intestinal villi were disordered, and the inflammatory cells infiltrated. The positive expression of ROS, and the contents of Fe2+ and MDA were elevated (P<0.05), the levels of GSH, SOD and ATP decreased (P<0.05), the mRNA expression of Nrf2 and GPX4 and the protein expression of Nrf2, GPX4 and SLC7A11 were reduced (P<0.05), while the mRNA expression of Keap1 and the protein expression of Keap1 and ACSL4 were elevated (P<0.05). When compared with the model group, the rats in the EA group showed the increase in food intake, body weight, gastric emptying rate and intestinal propulsion rate (P<0.05). In the duodenal tissue, the structure of the intestinal mucosa was intact basically, without inflammatory cell infiltration in the lamina propria. The positive expression of ROS, and the contents of Fe2+ and MDA were dropped (P<0.05), the contents of GSH, SOD and ATP rose (P<0.05), the mRNA expression of Nrf2 and GPX4 and the protein expression of Nrf2, GPX4 and SLC7A11 were elevated (P<0.05), while the mRNA expression of Keap1 and the protein expression of Keap1 and ACSL4 were reduced (P<0.05). Conclusion:Electroacupuncture at "Zusanli" (ST36) and "Taichong" (LR3) alleviates lipid peroxidation and oxidative stress injury in the duodenum of FD rats, maintains intracellular iron homeostasis, and inhibits ferroptosis probably by regulating Keap1/Nrf2/GPX4 pathway, so as to attenuate FD.

Efferocytosis—the phagocytic clearance of apoptotic cells—is central to tissue homeostasis and the active resolution of inflammation. Although its mechanistic basis and disease relevance have been studied in isolation, no review has comprehensively integrated neutrophil efferocytosis mechanisms, their pathophysiological roles across major chronic inflammatory gastrointestinal diseases, and natural product-based therapeutic strategies—a gap this work addresses. We systematically describe the efferocytic recognition cascade, encompassing find-me signals, eat-me signals (including phosphatidylserine and the underappreciated plasminogen/M6P-IGF2R axis), and don’t-eat-me checkpoints (CD47-SIRPα). We clarify that efferocytosis is not restricted to M2-polarized macrophages—M0 and M1 macrophages also participate—but that polarization state critically determines the pro-resolving coupling of downstream signaling. We analyze shared and disease-specific efferocytic defect mechanisms in inflammatory bowel disease, chronic gastritis, NAFLD/NASH, and pancreatitis, identifying IL-10R signaling failure, receptor shedding, CD47 upregulation, and SPM deficiency as convergent pathological nodes. Against this backdrop, we critically evaluate natural product strategies—flavonoids, polyphenols, alkaloids, terpenoids, polysaccharides, and omega-3 fatty acids—targeting these nodes, with explicit grading of evidence levels. Translational challenges and the potential of single-cell sequencing, spatial transcriptomics, and patient-derived organoid co-culture systems are also discussed. Restoring efferocytosis represents a mechanistically grounded therapeutic frontier for chronic gastrointestinal disease.

ObjectiveTo clarify the pathway by which electroacupuncture at “Taichong” （LR3） and “Zusanli” （ST36） alleviates low-grade duodenal inflammation in functional dyspepsia （FD） rats via regulating the Hippo/Yes-associated protein （YAP） signaling pathway.MethodsA total of 21 male SD rats （SPF grade） were enrolled and randomly divided into the blank group， the model group， and the electroacupuncture （EA） group （n = 7）. The FD model was established through a combined induction strategy involving simultaneous administration of exhaustive swimming， tail-clamping stimulation， and food restriction/overeating protocols， with continuous intervention lasting 21 days. Rats in the EA group received EA stimulation at LR3 and ST36， once daily for 20 min， 6 consecutive days followed by 1-day rest each course ， with 2 courses administered in total. The general physical conditions and body weight of rats in each group were monitored throughout model establishment and treatment. Upon completion of intervention， the 3-h food intake， gastric emptying rate and small intestinal transit rate of rats were measured. HE staining was performed to observe pathological changes in duodenal mucosa. ELISA was adopted to detect serum levels of motilin （MLT） and gastrin （GAS）. Western blot was used to quantify the protein expressions of YAP， transcriptional coactivator with PDZ-binding motif （TAZ）， phosphorylated （p）-YAP and p-TAZ in duodenal tissues. Immunohistochemistry was applied to determine the positive expression of interleukin （IL）-1β， IL-6 and tumor necrosis factor-α （TNF-α） in duodenum. Immunofluorescence staining was conducted to detect the positive expression of Occludin and zonula occludens-1 （ZO-1） in duodenal tissues. Quantitative real-time PCR was utilized to test the mRNA expression levels of YAP， TAZ， B-cell lymphoma-2 （Bcl-2） and Bcl-2-associated X protein （Bax） in duodenum. TUNEL staining was carried out to assess the apoptotic rate of duodenal epithelial cells.ResultsCompared with the blank group， rats in the model group exhibited severe lethargy， manifested as narrowed eyes， curled recumbency， dry and messy fur， and loose stools； the body weight， 3-h food intake， gastric emptying rate and small intestinal transit rate were markedly decreased （P<0.05， P<0.01）； massive inflammatory infiltration was observed in the lamina propria of duodenal tissues； serum MLT and GAS concentrations were significantly reduced （P<0.01）； the protein expression ratios of p-YAP/YAP and p-TAZ/TAZ in duodenum were notably elevated （P<0.01）； the positive expression of IL-1β， IL-6 and TNF-α in duodenal tissues was upregulated （P<0.01）. The mean fluorescence intensity of Occludin and ZO-1 in duodenum was remarkably lowered （P<0.01）. The mRNA level of Bax in duodenal tissues was significantly increased （P<0.01）， while the mRNA expressions of YAP， TAZ and Bcl-2 were distinctly downregulated （P<0.01）. The apoptotic rate of intestinal epithelial cells was markedly higher （P<0.01）. After EA intervention， relative to the model group， rats in the EA group showed improved mental state， enhanced locomotor activity， glossy fur and formed stools， the inflammatory infiltration in the duodenal lamina propria was alleviated， and all the indicators above were reversed （P<0.01， P<0.05）.ConclusionElectroacupuncture at LR3 and ST36 can effectively relieve symptoms of FD， improve the general physical status and suppress low-grade duodenal inflammation in FD rats. Its therapeutic mechanism may be associated with the Hippo/YAP signaling pathway.

Objective To observe the effect of electroacupuncture(EA)at"Tianshu"(ST25)and"Zusanli"(ST36)on NOD-like receptor protein 3(NLRP3)/cysteine aspartate specific protease 1(Caspase-1)/gasdermin D(GSDMD)pyroptosis signaling pathway in ulcerative colitis(UC)mice,so as to explore its mechanism in improving UC by protecting intestinal barrier.Methods Fifty male C57BL/6 mice were randomly divided into normal,model,EA,sham acupuncture and medication groups,with 10 mice in each group.The UC mouse model was established by 3%DSS solution free drinking for 7 consecutive days.The mice in the EA group received EA(2 Hz/10 Hz,0.2 mA)at bilateral ST25 and ST36 for 20 min,while the mice in the sham acupuncture group received only sham acupuncture(light and shallow acupunture at ST25 and ST36).Mice in the medication group were orally administered mesalazine(33.4 g/kg)solution.All the interventions were performed once daily for a total of 7 days.The changes of body weight,stool shape and hematochezia of mice,the disease activity index(DAI)score,and the length of colon were recorded.The intestinal mucosal permeability was observed by in vivo small animal imaging system.HE staining was used to observe the pathological changes of colon tissue.TUNEL staining was used to observe the apoptosis of colon cells.The contents of interleukin(IL)-18 and IL-1β in serum were detected by ELISA.The average fluorescence intensity of tumor necrosis factor-α(TNF-α)and IL-6 in colon tissue was detected by immunofluorescence.The positive expression of IL-18 and IL-1β in colon tissue was detected by immunohistochemistry.The relative expression levels of zonula occludens-1(ZO-1),Occludin,NLRP3,Caspase-1 and GSDMD in colon tissue were detected by Western blot.The mRNA expressions of NLRP3,Caspase-1 and GSDMD in colon tissue were detected by qPCR.Results After modeling,the DAI,inflammatory infiltration,number of apoptotic cells,fluorescence intensity of TNF-α,IL-6 and FITC,positive expression rate of IL-18 and IL-1β,mRNA and protein expression levels of NLRP3,Caspase-1 and GSDMD,serum IL-18 and IL-1β contents were significantly increased(P<0.01)in the model group relevant to the normal group.At the same time,the colon length,ZO-1 and Occludin protein expression were significantly reduced(P<0.01).The increased DAI,inflammatory infiltration,number of apoptotic cells,fluorescence intensity of TNF-α,IL-6 and FITC,positive rate of IL-18 and IL-1β,mRNA and protein expression levels of NLRP3,Caspase-1 and GSDMD,serum IL-18 and IL-1β contents,and the decreased colon length,ZO-1 and Occludin protein expression were all reversed after the EA and medication interventions compared with the model group and in the EA group than in the sham acupuncture group(P<0.01,P<0.05).Conclusion EA can protect the intestinal mucosal permeability in UC mice,which may be related to its functions in regulating the NLRP3/Caspase-1/GSDMD axis and inhibiting pyroptosis,thereby alleviating the inflammatory injury of intestinal mucosa.

This study aimed to investigate the effect and mechanism of Buyang Huanwu Decoction in regulating endoplasmic reticulum stress via the inositol-requiring enzyme 1α(IRE1α)/apoptosis signal-regulating kinase 1(ASK1)/c-Jun N-terminal kinase(JNK) pathway to improve neurological function in rats with cerebral ischemia/reperfusion injury(CIRI). SPF-grade male sprague-dawley(SD) rats were randomly divided into Sham group, model group, Buyang Huanwu Decoction group, and edaravone group. Except for the Sham group, the other groups were subjected to the modified suture method to establish a middle cerebral artery occlusion/reperfusion(MCAO/R) model. After treatment, neurological function was assessed using the Zea Longa scoring system. Gait analysis was used to detect the motor function. Detection of relative infarct area in brain tissue using 2,3,5-triphenyltetrazolium chloride(TTC) staining. Nissl staining was used to observe the structure of neuronal cells. Western blot and real-time fluorescence quantitative PCR(RT-qPCR) were used to detect IRE1α, ASK1, JNK, B cell lymphoma-2(Bcl-2), Bcl-2 related X protein(Bax), and Caspase-3 in the brain tissue. Immunohistochemistry was used to detect the positive expression of IRE1α, ASK1, and JNK. Immunofluorescence was used to detect the fluorescence expression levels of Bax, Bcl-2, and Caspase-3. The results showed that compared with the Sham group, the model group exhibited increased neurological scores(P&lt;0.01), increased ratio of ground contact area and strength in both forelimbs(P&lt;0.01), enlarged relative infarct area of brain tissue(P&lt;0.05), and a reduced number of Nissl staining-positive cells(P&lt;0.01). The protein and mRNA expression levels of IRE1α, ASK1, JNK, Bax, and Caspase-3 in brain tissue were significantly elevated, while those of Bcl-2 were decreased(P&lt;0.05). Compared with the model group, both the Buyang Huanwu Decoction group and edaravone group showed reduced neurological scores(P&lt;0.05), decreased ratio of ground contact area and strength in both forelimbs(P&lt;0.05), smaller relative infarct area(P&lt;0.05), alleviated neuronal damage, and increased number of Nissl staining-positive cells(P&lt;0.05). The expression levels of IRE1α, ASK1, JNK, Bax, and Caspase-3 protein and mRNA in brain tissue were significantly reduced, while those of Bcl-2 were significantly increased(P&lt;0.05). The results indicated that Buyang Huanwu Decoction can effectively improve brain injury in CIRI rats, and its mechanism of action may be related to regulating the endoplasmic reticulum stress IRE1α/ASK1/JNK signaling pathway.

Background: Buyang Huanwu decoction (BHD) is a traditional Chinese medicine herbal formula used for treating hypertension, particularly in the later stages of hypertension when it is associated with intracerebral hemorrhage. This study aims to investigate the treatment mechanism of BHD to provide a basis for its clinical application in hypertension treatment. Methods: Network pharmacology analysis and cell culture experiments were performed to explore the potential proteins and mechanisms of action of BHD against hypertension. Bioactive compounds related to BHD were screened, and relevant targets associated with hypertension and BHD were retrieved. Molecular docking technology was used to identify the effective signaling pathway based on the Kyoto Encyclopedia of Genes and Genomes and protein -protein interaction network cores. Lastly, the effects and mechanisms of BHD on salt-sensitive hypertensive endothelial cells were investigated. Results: Ninety-three potential therapeutic targets for BHD and salt-sensitive hypertension were found to be closely associated with the PI3K/Akt/eNOS signaling pathway and oxidative stress. Cell experiments further indicated the pivotal role of endothelial cells in hypertension, and validation analysis showed that BHD significantly preserved cell morphology, suppressed oxidative stress reactions, activated the PI3K/Akt/eNOS signaling pathways, preserved normal endothelial cell function, and reduced cell apoptosis. Conclusion: BHD effectively activates the PI3K/Akt/VEGF signaling pathway, attenuates oxidative stress-induced injury in endothelial cells exposed to high salt levels, and mitigates apoptosis, supporting the use of traditional Chinese medicine BHD in the treatment of salt-sensitive hypertension.

目的 研究补阳还五汤调控上皮钠通道(ENaC)泛素化,保护人肾小管上皮细胞(HK2)钠代谢异常作用机制.方法 采用高盐(150mmol/L)干预HK2细胞24h,诱导细胞损伤.加入不同剂量的补阳还五汤(0.5％,1％,2％)干预24h,收集细胞.用Hoechst33342染色,高内涵观测细胞数量;荧光定量PCR检测SGK1、NEDD4-2、ENaC mRNA含量;Wes全自动蛋白表达分析系统检测SGK1、NEDD4-2、ENaC的蛋白表达.结果 高盐组造模后,细胞数量显著减少,细胞活性变差;SGK1、ENaC mRNA含量及蛋白表达显著升高(P＜0.05);NEDD4-2 mRNA及蛋白含量显著降低(P＜0.05).补阳还五汤干预治疗,可以显著增加细胞数量及活性,抑制SGK1表达,增加泛素连接酶NEDD4-2含量,促进ENaC泛素化降解,从而减少HK2细胞钠离子重吸收,差异具有统计学意义(P＜0.05).结论 补阳还五汤能激活HK2细胞泛素化系统,通过促进ENaC泛素化降解,减少细胞钠离子重吸收,从而起到盐敏感高血压肾脏保护作用.

观察补阳还五汤调控炎症信号通路对肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)诱导的人脐静脉内皮细胞(hu-man umbilical vein endothelial cells,HUVECs)损伤的影响.采用10 ng/mL TNF-α建立细胞损伤模型,使用不同浓度的补阳还五汤(0.5％、1％、2％)干预处理24 h后收集细胞.通过Hoechst 33342染色高内涵观测细胞数量,Western blot检测炎症信号通路NF-κB p65和IκB的蛋白表达水平,逆转录-聚合酶链反应(reverse transcription-polymerase chain reaction,RT-PCR)检测相关炎症因子NF-κB、IκB、ICAM-1、VCAM-1、MCP-1的mRNA表达.结果表明,应用10 ng/mL TNF-α预处理HUVECs 24 h可明显降低细胞存活率,细胞数量明显减少,NF-κB p65蛋白表达升高,IκB蛋白和mRNA表达降低,NF-κB、ICAM-1、VCAM-1、MCP-1 mRNA表达水平增加(P<0.05).补阳还五汤干预处理后,细胞数量明显增加,且抑制了NF-κB p65及炎症因子NF-κB、ICAM-1、VCAM-1、MCP-1的高表达,IκB蛋白和mRNA表达水平均显著下降(P<0.05).补阳还五汤通过抑制NF-κB炎症信号通路的激活,降低了炎症因子的高表达,对TNF-α诱导的HUVECs损伤起到保护作用.

基于课程思政理念,将生命教育、环保教育、安全教育、规则教育、科学精神与学术道德、社会责任感以及人文关怀和心理疏导等思政元素与实验室安全教学实践有机结合,全面贯彻党的教育方针.落实立德树人根本任务,使学生树立正确的人生观、价值观,实现思想与价值的引领,更好地发挥实验室的育人功能,提升实验室安全管理能力和服务水平.

目的 观察补阳还五汤对TNF-α诱导人脐静脉内皮细胞（HUVECs）损伤的保护作用。方法 以TNF-α10ng/ml、24h建立血管内皮细胞损伤模型，通过加入不同浓度的补阳还五汤（0.5%、1%、2%）进行干预，采用CCK-8法检测补阳还五汤对细胞增殖的保护作用，流式细胞仪检测各组细胞的凋亡情况，荧光定量PCR检测细胞NLRP3、ASC、Caspase-1mRNA的表达情况，Wes TM 全自动蛋白印迹定量分析系统检测NF-κB的蛋白表达。结果 与正常组比较，模型组数目明显减少，细胞活性显著降低（P＜0.05）;各给药组的细胞增殖有显著差异（P＜0.05）;与模型组比较，补阳还五汤高、中、低组均可以减少HUVECs的凋亡（P＜0.05）;抑制NLRP3炎症小体及NLRP3、ASC、Caspase-1的表达（P＜0.05）;降低了NF-κB蛋白的表达（P＜0.05）。结论 补阳还五汤能明显抑制TNF-α诱导的HUVECs凋亡发挥炎症的保护作用。

以科研项目为依托,针对当前高校对本科生的创新创业教育存在的问题做简要分析并提出相应建议,从而更好地提高学生的创新创业能力.

目的 通过观察防己黄芪汤对肥胖性高血压模型大鼠肾脏组织过氧化物酶增殖物激活受体γ(PPARγ)/脂联素(APN)/腺苷酸活化蛋白激酶(AMPK)信号通路的影响,探讨防己黄芪汤对肥胖性高血压模型大鼠的肾脏保护机制.方法 10只Wistar-kyoto(WKY)大鼠为正常组,60只雄性自发性高血压(SHR)大鼠按随机数字表法分为模型组、肥胖模型组、中药低剂量组、中药中剂量组、中药高剂量组、西药组(10只/组).以高脂饲料喂养建立肥胖性高血压大鼠模型,期间监测大鼠体质量和尾动脉收缩压变化,当除正常组与模型组外的其余组大鼠体质量超过正常组体质量20％时,提示肥胖性高血压大鼠模型复制成功.造模成功后,予以药物灌胃干预治疗,每日1次,治疗周期为5周.采用荧光定量PCR法检测大鼠肾脏组织PPARγ、APN、AMPK mRNA表达水平,蛋白质免疫印迹法(WB)检测大鼠肾脏组织内PPARγ和APN的蛋白含量变化.结果 模型组和肥胖模型组大鼠PPARγ、APN、AMPK mRNA表达及PPAR γ、APN的蛋白表达与正常组相比均有所下调(P＜0.05);肥胖模型组大鼠PPARγ、APN、AMPK mRNA表达及PPARγ、APN的蛋白表达与模型组相比亦明显下调(P＜0.05);药物治疗组大鼠PPARγ、APN、AMPK mRNA表达及PPAR γ、APN的蛋白含量与肥胖模型组和模型组相比均显著提高(P＜0.05),且中药中剂量组提高最为明显(P＜0.05).结论 防己黄芪汤通过调节肾脏组织PPAR γ/APN/AMPK信号通路,发挥减重与降压双重作用,保护肾脏,从而延缓肥胖性高血压发展进程.

目的 观察电针"足三里"对脾虚大鼠心肌细胞线粒体能量代谢、线粒体自噬的影响.方法 48只SD大鼠,随机分为正常对照组、模型组、足三里组、非经非穴组,每组12只.采用三因素复合法复制脾虚证模型,持续14 d.足三里组针刺大鼠双侧足三里穴,非经非穴组针刺大鼠双侧髂嵴上非经非穴点,电针治疗10 d.高效液相色谱法检测大鼠心肌细胞三磷酸腺苷(ATP)、二磷酸腺苷(ADP)以及磷酸腺苷(AMP)的含量;Western blotting法检测大鼠心肌细胞腺苷酸活化蛋白激酶(AMPK)、磷酸化AMPK(p-AMPK)、微管相关蛋白1轻链3-I(LC3-I)以及LC3-II蛋白的表达;利用透射电镜观察大鼠心肌细胞线粒体及线粒体自噬体的超微结构.结果 与正常对照组相比,模型组、足三里组以及非经非穴组大鼠心肌AMP/ATP、LC3-II/LC3-I均明显上调(P﹤0.01);模型组大鼠心肌p-AMPK/AMPK有所上调(P﹤0.05),足三里组大鼠心肌p-AMPK/AMPK显著上调(P﹤0.01).与模型组相比,足三里组大鼠心肌LC3-II/LC3-I显著上调(P﹤0.01).模型组大鼠心肌线粒体损伤明显,足三里组线粒体损伤有所改善,见大量的线粒体自噬体.结论 电针"足三里"可能通过激活脾虚大鼠心肌细胞AMPK,调节线粒体能量代谢、提高线粒体自噬水平,对脾虚大鼠起到干预作用.

针对中医药创新团队建设存在的问题,从团队规模建设、团队精神培养等方面提出相应解决措施.

目的:观察补阳还五汤对Dahl盐敏感大鼠介导的高血压模型大鼠心肌组织AngⅡ/AT1R与PI3K/AKt信号通路的作用.方法:选取7周龄盐抵抗(SS)大鼠和盐敏感大鼠(DS)随机分为正常组、模型组、中药组、西药组4组各10只.各组大鼠给予8％Nacl高盐饲料喂养,期间采用智能无创血压计检测大鼠尾动脉收缩压(SBP),高血压模型大鼠造模成功后,停止高盐喂饲改为普通饲料喂养,中药组和西药组分别给予补阳还五汤和缬沙坦灌胃治疗,每日1次,连续5周.治疗结束后取大鼠左心室心肌组织,WESTERN BLOT和ELISA法测定AT1R和AngⅡ含量表达,荧光定量PCR法检测PI3K、AKt的mRNA表达.结果:与正常组比较,模型组大鼠AT1R和AngⅡ的含量明显升高,PI3K、AKt的mRNA表达显著降低;与模型组比较,中药组和西药组大鼠AT1R和AngⅡ的含量显著降低,PI3K、AKt的mRNA表达显著升高,且西药组优于中药组.结论:补阳还五汤通过抑制AngⅡ/AT1R轴激活,缓解AngⅡ/AT1R与PI3K/AKt信号通路的失衡状态,降低血压,保护心肌组织的损伤,延缓高血压对靶器官的损伤.

Objective: To observe the effect of electroacupuncture at bilateral "Zusanli (ST36) " on the expressions of nuclear respiratory factor 1 (NRF1) and 2 (NRF2) gene and protein in muscle tissue of rats with spleen Qi deficiency model. Methods: Thirty-two male SD rats were randomly divided into normal group, spleen Qi deficiency group, Zusanli (ST36) group and non-acupoint group, and the model of spleen Qi deficiency syndrome was established by the composite methods of improper diet and overstrain except the normal group. The rats were treated with electroacupuncture at the bilateral "Zusanli (ST36) " and non-acupoint intervention seven days after the model was successfully established. The changes of NRF1 and NRF2 mRNA and protein expression in skeletal muscle and gastric smooth muscle were detected by fluorescence quantitative PCR method and Western blot (WB). Results: The expressions of NRF1 and NRF2 protein and mRNA in skeletal muscle and gastric smooth muscle of spleen Qi deficiency group were significantly lower than those of normal group, and the level of its' expression had increased in Zusanli (ST36) group, there was no significant difference between spleen Qi deficiency group and non-acupoint group (P<0.01). Conclusion: Electroacupuncture at "Zusanli (ST36) " can improve spleen Qi deficiency by participating in the regulation of mitochondrial energy metabolism through regulating the abnormal expressions of NRF1 and NRF2 genes and proteins in muscle tissue of rats with spleen Qi deficiency.

目的:观察补阳还五汤对Dahl盐敏感大鼠介导的高血压模型大鼠肾脏组织ACE/AngⅡ/AT1R轴与ACE2/Ang(1-7)/MasR轴表达的影响,探讨补阳还五汤对高血压模型大鼠肾脏组织RAS系统平衡作用机制.方法:选取7周龄盐抵抗(SS)大鼠10只分为正常组,30只盐敏感大鼠(DS)随机分为模型组、中药组、西药组3组,每组10只.各组大鼠予以8％ Nacl高盐饲料喂养,期间采用智能无创血压计检测大鼠尾动脉收缩压(SBP),高血压模型大鼠造模成功后,停止高盐喂饲,改为普通饲料喂养,中药组和西药组分别给予补阳还五汤和缬沙坦灌胃治疗,1次/d,连续5周.治疗结束后取大鼠肾脏组织,荧光定量PCR法检测各组ACE、AT1R、ACE2、MasR的mRNA表达,ELISA法检测各组AngⅡ、Ang(1-7)含量表达,Western Blot检测各组AT1R的蛋白表达.结果:与正常组相比,模型组大鼠ACE、AT1R的mRNA表达显著上升(P＜0.05),ACE2、MasR的mRNA表达显著下降(P＜0.05),AngⅡ的含量明显升高(P＜0.05),Ang(1-7)的含量明显下降(P＜0.05),AT1R的蛋白表达明显上升(P＜0.05);与模型组比较,中药组和西药组大鼠ACE、AT1R的mRNA表达显著下降(P＜0.05),ACE2、MasR的mRNA表达显著上升(P＜0.05),AngⅡ的含量显著下降(P＜0.05),Ang(1-7)的含量显著上升(P＜0.05),AT1R的蛋白表达显著下降(P＜0.05);与中药组相比,西药组大鼠ACE、AT1R的mRNA表达显著下降(P＜0.05),ACE2、MasR的mRNA表达显著上升(P＜0.05),AngⅡ的含量显著下降(P＜0.05),Ang(1-7)的含量显著上升(P＜0.05),AT1R的蛋白表达显著下降(P＜0.05).结论:补阳还五汤可能通过抑制ACE/AngⅡ/AT1R轴的表达,促进ACE2/Ang(1-7)/MasR轴的表达,进而维持RAS平衡的状态,从而降低血压,保护肾脏组织的损伤,延缓高血压对靶器官的损伤.

Objective: To investigate the effect of electroacupuncture at Zusanli (ST36) on protein and gene expression of small peptide transporter (PepT1) in small intestinal mucosa of rats with deficiency of spleen Qi.Methods: Forty male SD rats were randomly divided into normal group, spleen Qi deficiency group, Zusanli (ST36) group and non-meridian non-acupoint group.All rats were fed in SPF level animal experimental center.The normal diet was given to the normal group, and the other three groups were treated with irregular diet and overfatigue combined method to establish the model of spleen Qi deficiency syndrome in rats.After the model was established successfully, the Zusanli (ST36) group was treated with electroacupuncture at Zusanli (ST36), and the rats of non-meridian non-acupoint group were treated with non-meridian and non-acupoint intervention for 7 days. We observed the changes of thymus index and spleen index of rats in each group, the propelling rate of small intestine in each group by HE staining. The protein content of PepT1 in small intestinal mucosa of rats was detected by Western blotand the mRNA expression of PepT1 in small intestinal mucosa of rats was detected by fluorescence quantitative PCR method.Results: The weight of thymus and spleen and the rate of small intestine propulsion in spleen deficiency group were significantly lower than those in normal group. The results of HE staining in Zusanli (ST36) group compared with spleen deficiency group showed that the histological morphology of Zusanli (ST36) group was better than that of spleen Qi deficiency group.Compared with the normal group, the levels of PEPT1 protein and gene expression in the small intestinal mucosa of the spleen Qi deficiency group were significantly lower than those of the normal group (P<0.05), and those of the spleen Qi deficiency group were significantly lower than those of the spleen Qi deficiency group.In Zusanli (ST36) group, the expression of PEPT1 protein and gene in small intestinal mucosa was increased (P<0.05), but no significant difference was found in non-acupoint group (P<0.05). Conclusion: Electroacupuncture at Zusanli (ST36) can regulate the abnormal expressions of PEPT1 protein and gene in the small intestinal mucosa of spleen Qi deficiency rats, participate in the absorption of protein by the small intestine, and then improve the spleen Qi deficiency syndrome.

目的:观察电针双侧“足三里”穴对脾气虚模型大鼠骨骼肌组织PGC-1 α/SIRT3信号通路表达的影响.方法:将32只SD雄性大鼠随机分为空白组、脾气虚组、足三里组、非经非穴组.除空白组外,其余3组均采用劳倦过度和不规则饮食复合法建立脾气虚证大鼠模型.造模成功后,足三里组给予电针双侧“足三里”穴治疗,非经非穴组予以电针双侧非经非穴点治疗,每日1次,每次20 min,共治疗7d.观察各组大鼠的一般状态,采用大小鼠抓力测定仪测量大鼠前肢抓力;采用荧光定量PCR法检测大鼠骨骼肌PG-1α、ERRα、SIRT3及SOD2的mRNA表达水平;采用Western blot检测大鼠骨骼肌PGC-1α、ERRα、SIRT3及SOD2的蛋白表达水平.结果:与空白组相比,脾气虚组和非经非穴组大鼠形体消瘦,体质量下降,进食量减少,皮毛枯槁脱落,懒动,大便稀溏;抓力显著下降(P＜0.05);骨骼肌组织中PGC-1α、ERRα、SIRT3及SOD2的mRNA和蛋白表达水平均明显降低(P＜0.05).与脾气虚组相比,足三里组大鼠活动性增加,进食量增加,体质量略增加,被毛掉落减少,便溏情况有所好转;大鼠抓力明显增大(P＜0.05);骨骼肌组织中PGC-1α、ERRα、SIRT3及SOD2的mRNA和蛋白表达水平均明显升高(P＜0.05),非经非穴组未见显著性差异(P＞0.05).结论:电针“足三里”穴可以调节脾气虚大鼠骨骼肌内PGC-1 α/SIRT3信号通路的异常表达,参与线粒体生物合成及抗氧化的调控作用进而发挥健脾益气作用.

Objective: To observe the effect of electroacupuncture at Zusanli (ST36) on the gene and protein expression of sodium dependent glucose transporter (SGLT1) and glucose carrier protein (GLUT2) in the epithelium of small intestinal mucosa of rats with spleen Qi deficiency. Methods: Forty SD rats were divided into two groups. Male rats were randomly divided into normal group, spleen Qi deficiency group, Zusanli (ST36) group, non-meridian non-acupoint group, 10 rats in each group. All rats were raised in SPF level animal experimental center. The other three groups were used to establish the rat model of spleen Qi deficiency by the method of overfatigue and irregular diet. After the model was established, the rats in Zusanli (ST36) group and non-meridian non-acupoint group were treated respectively with Zusanli (ST36) group and non-meridian non-acupoint group. Electroacupuncture at Zusanli (ST36) was performed for 7 days without intervention at non-acupoint point. The morphological changes of small intestine mucosa were observed by HE staining method, and the expressions of SGLT1 and GLUT2 in rat small intestinal mucosa epithelium were detected by fluorescence quantitative PCR method. The protein contents of SGLT1 and GLUT2 in small intestinal mucosa of rats were detected by Western blot. Results: The intestinal mucosal tissue was partially damaged in spleen Qi deficiency group and recovered to some extent in Zusanli (ST36) group. The levels of SGLT1 and GLUT2 protein and gene expression in small intestinal mucosa of rats with deficiency of spleen Qi and non-acupoints were significantly lower than those of normal group (P ＜ 0.05), and the expression levels of SGLT1 and GLUT2 protein and gene in small intestinal mucosa of Zusanli (ST36) group were significantly lower than those of the normal group (P ＜ 0.05), and those of Zusanli (ST36) group were significantly lower than those of the normal group (P ＜ 0.05). There was no significant difference in spleen Qi deficiency group (P ＜0.05), but no significant difference was found in non-meridian non-point group (P ＜ 0.05). Conclusion: Electroacupuncture at Zusanli (ST36) can regulate the abnormal expressions of SGLT1 and GLUT2 gene and protein in the epithelium of small intestine mucosa of rats with spleen Qi deficiency, and participate in the absorption of glucose in the small intestine and then improve the spleen Qi deficiency syndrome.