ObjectiveTo investigate the regulatory effects and underlying mechanisms of Liuhuang Zhike prescription （LHZK） on blood glucose in type 2 diabetic db/db mice based on the AMP-activated protein kinase/protein kinase B/glycogen synthase kinase-3β （AMPK/Akt/GSK-3β） signaling pathway. MethodsDb/db mice were used as the model animals， and db/m mice served as the blank control. Forty db/db mice were randomly divided into the model group， metformin group （0.14 g·kg^-1）， and low-， medium-， and high-dose （4.11， 8.21， 16.43 g·kg^-1） LHZK groups， with 8 mice in each group. The db/db mice in the metformin and LHZK groups were administered the corresponding drugs by gavage， while the blank control and model groups were given distilled water by gavage once daily for 8 consecutive weeks. Food intake， water consumption， body weight， and fasting blood glucose （FBG） were measured weekly. An automatic biochemical analyzer was used to determine glycated serum protein （GSP）， serum triglycerides （TG）， total cholesterol （TC）， high-density lipoprotein cholesterol （HDL-C）， and low-density lipoprotein cholesterol （LDL-C） levels. Hematoxylin-eosin （HE） staining was used to observe pathological morphological changes in the liver and pancreatic tissues. Oil red O staining was used to assess lipid accumulation in liver tissue. The anthrone colorimetric method was used to determine hepatic glycogen content. Real-time quantitative PCR （Real-time PCR） was used to detect the mRNA expression levels of insulin receptor substrate-1 （IRS-1）， Akt2， phosphoenolpyruvate carboxykinase （PEPCK）， and glucose-6-phosphatase （G6Pase） in liver tissue. Western blot was used to detect the protein expression of AMPKα， phosphorylated AMPKα （p-AMPKα）， GSK-3β， p-GSK-3β， glycogen synthase （GS）， and phosphorylated GS （p-GS） in liver tissue. ResultsCompared with the blank control group， the model group showed significantly increased food intake， water consumption， body weight， FBG， and GSP levels （P<0.01）. Pancreatic islets exhibited marked parenchymal cell hyperplasia and interstitial inflammatory cell infiltration. Liver tissue showed obvious steatosis， accompanied by a compensatory increase in hepatic glycogen content （P<0.01）. Hepatic G6Pase mRNA expression was increased， while IRS-1 and Akt2 mRNA expression levels were significantly decreased （P<0.01）. The p-AMPKα/AMPKα protein expression ratio showed a decreasing trend， whereas the p-GSK-3β/GSK-3β and p-GS/GS protein expression ratios were significantly increased （P<0.01）. Compared with the model group， food intake and water consumption showed decreasing trends in all treatment groups. Food intake was significantly reduced in the low- and high-dose LHZK groups and in the metformin group （P<0.05， P<0.01）， and water consumption was significantly reduced in the low-dose LHZK group and in the metformin group （P<0.05， P<0.01）. No statistically significant differences in body weight were observed among the LHZK groups， whereas body weight in the metformin group was significantly increased （P<0.05， P<0.01）. FBG showed a decreasing trend in all treatment groups， with significant decreases in the low-dose LHZK group and the metformin group （P<0.05， P<0.01）. GSP levels were significantly reduced in the low-dose LHZK group and in the metformin group （P<0.05， P<0.01）. Hepatic steatosis and pancreatic pathological injury were alleviated to varying degrees in all treatment groups. Hepatic glycogen content further increased in all treatment groups， with significant increases in the medium- and high-dose LHZK groups （P<0.05）. Real-time PCR results showed that all treatment groups downregulated the mRNA expression of G6Pase and PEPCK in the liver tissues of db/db mice， with significant downregulation of PEPCK mRNA in the low-dose LHZK and metformin groups （P<0.01）. Meanwhile， all treatment groups upregulated IRS-1 and Akt2 mRNA expression， with the most pronounced upregulation observed in the medium-dose LHZK group （P<0.01）. The p-AMPKα/AMPKα protein expression ratio was significantly increased in the low- and medium-dose LHZK groups （P<0.01）. The p-GSK-3β/GSK-3β protein expression ratio was significantly increased in all treatment groups （P<0.05， P<0.01）， whereas the p-GS/GS protein expression ratio was significantly decreased in all treatment groups （P<0.01）. ConclusionLHZK effectively reduces FBG and GSP levels in type 2 diabetic mice and improves hepatic steatosis and pancreatic islet pathological injury. Its hypoglycemic mechanism may be associated with regulation of the AMPK/Akt/GSK-3β signaling pathway and promotion of hepatic glycogen synthesis.

OBJECTIVE To form an expert consensus on the clinical application of parenteral direct thrombin inhibitors （DTIs） in patients during the perioperative period. METHODS Led by Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital （the Affiliated Hospital of UESTC）， a multidisciplinary working group was established. Through literature review and the Delphi method， clinical questions related to the rational perioperative use of parenteral DTIs were identified. A structured design was adopted using the “Population-Intervention-Comparison-Outcome” framework； systematic searches were conducted in CNKI， Medline， Embase and other databases. Relevant evidence from randomized controlled trials and cohort studies was included and synthesized. Evidence quality was assessed using the Grades of Recommendations Assessment，Development and Evaluation （GRADE） approach， and recommendations were formulated through multiple rounds of Delphi surveys and expert consensus meetings. RESULTS &CONCLUSIONS Seven recommendations （each with an expert consensus rate exceeding 90%） on the use of parenteral DTIs in perioperative patients were developed. These recommendations specify drug selection， dosing ranges， key monitoring points， and safety management strategies for parenteral DTIs in various scenarios， including the perioperative period of ventricular assist device implantation， the perioperative period of cardiac surgery， perioperative patients with lower-extremity atherosclerotic disease， the perioperative period of percutaneous coronary intervention in patients with acute coronary syndrome， the perioperative period of carotid artery stenting in patients with carotid stenosis， the perioperative period of patients with right heart thrombosis， and patients who develop related thrombosis and dysfunction after a central venous catheter insertion. In addition， warning and management pathways for perioperative bleeding and thrombotic events were proposed. This expert consensus， which is formulated based on the best available evidence， provides evidence-based guidance for standardized and individualized use of parenteral DTIs in perioperative period.

ObjectivePost-ischemic acute inflammation and the subsequent persistent dysregulation of the immune microenvironment represent major pathological drivers that aggravate neuronal injury and severely restrict functional recovery following ischemic stroke. Although current reperfusion therapies partially restore blood flow, they fail to effectively modulate the secondary inflammatory cascade and oxidative stress, which remain critical barriers to neurological restoration. To address this challenge, this study aimed to engineer and systematically evaluate a biomimetic nanosystem composed of transforming growth factor-β1 (TGF-β1)-loaded platelet membrane-camouflaged lipid nanoparticles (PLP). This nanosystem was designed to achieve dual lesion-targeted delivery and immune microenvironment remodeling. By verifying its spatiotemporal accumulation, anti-inflammatory activity, and neuroprotective efficacy, we sought to establish an integrated therapeutic strategy that simultaneously enables lesion targeting, immune regulation, and functional recovery after ischemic injury. MethodsThe physicochemical properties of PLP, including hydrodynamic particle size, zeta potential, structural stability, and morphology, were characterized using dynamic light scattering, zeta potential analysis, and transmission electron microscopy. The preservation of platelet membrane-derived adhesion and immunoregulatory proteins was confirmed by SDS-PAGE through comparative analysis of protein band profiles between PLP and native platelet membranes. The in vitro biological activities of PLP were evaluated using two complementary cellular models. LPS-induced M1-polarized RAW264.7 macrophages were employed to assess inflammatory modulation, while oxygen glucose deprivation/reperfusion (OGD/R)-induced BV2 microglial cells and SH-SY5Y neuronal cells were utilized to investigate neuroinflammatory regulation and neuronal protection. For in vivo validation, a transient middle cerebral artery occlusion (tMCAO) mouse model was established to mimic ischemia-reperfusion injury. The spatiotemporal biodistribution and lesion-targeting capability of the PLP were monitored through live fluorescence imaging. Therapeutic efficacy was comprehensively evaluated by triphenyltetrazolium chloride (TTC) staining, glial fibrillary acidic protein (GFAP) immunofluorescence analysis, body weight monitoring, and neurological severity score (NSS) assessment. ResultsPLP nanoparticles displayed a uniform spherical morphology, nanoscale particle size distribution, and stable negative surface charge, indicating favorable colloidal stability and circulation potential. SDS-PAGE results confirmed the effective retention of key platelet membrane proteins associated with endothelial adhesion, immune evasion, and inflammatory regulation, demonstrating the successful biomimetic construction. Optimal therapeutic concentrations were determined in OGD/R-induced BV2 cells, where PLP exhibited excellent cytocompatibility and anti-inflammatory activity.In vitro experiments demonstrated that PLP significantly inhibited the polarization of RAW264.7 macrophages toward the pro-inflammatory M1 phenotype and markedly reduced neuronal apoptosis under ischemia-reperfusion conditions. In vivo fluorescence imaging revealed that PLP rapidly accumulated in the ischemic brain hemisphere and maintained prolonged retention for up to 7 d, suggesting enhanced lesion-specific targeting and sustained drug release. Compared with control group, PLP treatment significantly reduced cerebral infarct volume, attenuated reactive astrogliosis, improved weight recovery, and accelerated neurological functional restoration, as reflected by significantly improved NSS scores. ConclusionThis study establishes a multifunctional biomimetic nanoplatform that integrates platelet membrane-mediated active targeting with the anti-inflammatory, antioxidative, and neuroprotective properties of TGF-β1. The PLP system enables rapid lesion homing and long-term retention while synergistically regulating the post-stroke inflammatory microenvironment by suppressing pro-inflammatory immune activation, reducing neuronal apoptosis, and limiting excessive astrocyte reactivity. Importantly, this study proposes a conceptually therapeutic paradigm that combines targeted delivery with immune microenvironment remodeling to achieve comprehensive neurovascular protection. These findings provide strong experimental evidence supporting the translational potential of biomimetic nanotherapeutics as next-generation precision interventions for ischemic stroke.

AIM To investigate the effects of Yiqi Juanbi Formula on chondrocyte pyroptosis in rat models of collagen-induced arthritis(CIA).METHODS Fifty rats were subcutaneously injected at the tail base with an emulsion containing equal volumes of bovine type Ⅱ collagen and incomplete Freund's adjuvant(IFA)to establish the CIA models.These rats were then randomly assigned to the model group,the methotrexate group(0.35 mg/kg),and the low-dose,medium-dose,and high-dose Yiqi Juanbi Formula groups(9.4,18.7,37.4 g/kg),in contrast to the ten intact rats serving in the normal control group.Following four weeks of intragastric administration,the rats had their general conditions observed;their joint swelling and arthritis indices measured;their ankle joint pathology assessed by HE staining;their serum levels of IL-1β,IL-18 and TNF-ɑ detected by ELISA;their mRNA expressions of NLRP3,Caspase-1,GSDMD,IL-1β,IL-18 and TNF-ɑ in ankle cartilage quantified by RT-qPCR;their protein expressions of NF-κB,NLRP3 and Caspase-1 in ankle cartilage analyzed by Western blot;and their NLRP3 and GSDMD positive expressions in ankle cartilage examined by immunohistochemistry.RESULTS Compared to the control group,the model group showed significantly increased joint swelling and arthritis indices(P＜0.01);elevated serum levels of IL-1 β,IL-18 and TNF-ɑ(P＜0.01);pathological changes including cartilage surface defects,reduced cell count,altered cellular morphology,irregular cell arrangement,and significant inflammatory cell infiltration in synovial tissue;upregulated mRNA expressions of NF-κB,NLRP3,Caspase-1,GSDMD,IL-1β,IL-18 and TNF-ɑ(P＜0.01)and increased protein expressions of NF-κB,NLRP3 and Caspase-1(P＜0.01)in ankle cartilage;enhanced positive expressions of NLRP3 and GSDMD in ankle cartilage(P＜0.01).Compared to the model group,the groups intervened with methotrexate or medium-or high-dose Yiqi Juanbi Formula exhibited reduced joint swelling and arthritis indices(P＜0.01);alleviated pathological damage in ankle joints;decreased serum levels of IL-1β,IL-18 and TNF-ɑ(P＜0.01);downregulated mRNA expressions of NF-κB,NLRP3,Caspase-1,GSDMD,IL-1β,IL-18 and TNF-ɑ(P＜0.05,P＜0.01),and reduced protein expressions of NF-κB,NLRP3 and Caspase-1(P＜0.05,P＜0.01)in ankle cartilage;and diminished positive expressions of NLRP3 and GSDMD in ankle cartilage(P＜0.01).CONCLUSION Yiqi Juanbi Formula alleviates inflammation in CIA rats,potentially by inhibiting the activation of the NF-κB/NLRP3/Caspase-1 signaling pathway,thereby suppressing chondrocyte pyroptosis.

AIM To evaluate the quality of Gegen Formula Granules.METHODS Linear calibration with two reference substances(LCTRS)was adopted in the predicting of retention time with puerarin and daidzein as internal standards.UPLC characteristic chromatograms were established.The contents of 3'-hydroxy puerarin,puerarin(internal standard),3'-methoxy puerarin,puerarin 6"-O-xyloside,puerarin apioside and daidzin were determined by quantitative determination analysis multi-components by a single marker(QAMS),after which their transfer rates were calculated.RESULTS Compared with relative retention time method,LCTRS demonstrated higher positional accuracy for characteristic peaks and wider application range for columns.There were 9 characteristic peaks in the characteristic chromatograms for 14 batches of formula granules and 15 batches of standard decoctions with the similarities of more than 0.95.The contents and transfer rates of various constituents in formula granules and standard decoctions were basically consistent.CONCLUSION The chemical constituents in formula granules and their standard decoctions of Puerariae lobatae Radix display good consistency,reliable preparation process is observable in the former.

Objective:To explore the prognostic value of artificial intelligence-based P53 and Ki67 detection in stage I non-mucinous adenocarcinoma(INMA)of lung.Methods:A retrospective analysis was made of patients treated by radical surgical resection for INMA of lung in the Department of Thoracic Surgery of Peking University First Hospital from Jan.2015 to Dec.2016,with complete clinicopathological and 5-year follow-up data.Immunohistochemical staining for P53 and Ki67 was performed on all cases and the index of P53 and Ki67 was calculated with the assistance of artificial intelligence(AI).The optimal cut-off values for P53 and Ki67 were determined using X-Tile software,and based on these values,the patients were divided into low-expression and high-expression groups.Pearson chi-square test and Fisher's exact test were used to compare the differences in clinicopathological characteristics between the different groups.Univariate and multivariate Cox regression analyses were performed to assess the impact of various indicators on 5-year overall survival(OS)and disease-free survival (DFS)for stage I INMA.The time-dependent receiver operating characteristic(ROC) curves and the area under the curve(AUC)was used to analyze the predictive performance of P53 and Ki67 for the prognosis of stage I INMA.Results:Among the 191 patients, the median follow-up time was 60(54, 60) months. The index of P53 and Ki67 were 0%-100% and 1.0%-78.0%,respectively. The X-Tile software revealed optimal cut-off values of 62% for P53 and 20% for Ki67.Then the patients were divided into P53 low-expression group (<62%), P53 high-expression (≥62%) group and Ki67 low-expression (<20%)group,Ki67 high-expression group (≥20%). High expression of P53 was associated with male ( χ2=12.45, P<0.001), smoking ( χ2=12.24, P<0.001), pTNM stage ( χ2=16.28, P<0.001), and histological grade ( P<0.001). High expression of Ki67 was associated with male ( χ2=17.33, P<0.01), smoking ( χ2=21.67, P<0.01), and histological grade ( P<0.001). Male ( HR=2.612, 95% CI: 1.173-5.815, P=0.019), smoking ( HR=2.651, 95% CI: 1.246-5.642, P=0.011), high pTNM stage ( HR=3.815, 95% CI: 1.792-8.122, P<0.001), high histological grade ( HR=5.277, 95% CI: 2.400-11.606, P<0.001), high P53 expression ( HR=5.950, 95% CI: 2.792-12.680, P<0.001), and high Ki67 expression ( HR=3.349, 95% CI: 1.554-7.221, P=0.002) were associated with poorer disease-free survival (DFS). Male ( HR=9.050, 95% CI: 1.113-73.586, P=0.039), smoking ( HR=8.428, 95% CI: 1.701-41.765, P=0.009), high histological grade ( HR=6.865, 95% CI: 1.756-26.834, P=0.006), high P53 expression ( HR=16.699, 95% CI: 3.369-82.761, P<0.001), and high Ki67 expression ( HR=7.558, 95% CI: 1.806-31.632, P=0.006) were associated with poorer overall survival. P53 high-expression was identified as an independent risk factor for both DFS ( HR=2.843, 95% CI: 1.192-6.778, P=0.018) and OS( HR=6.909, 95% CI: 1.202-39.720, P=0.030) in stage I INMA patients. The area under the time-dependent ROC curves for predicting 5-year overall survival after surgery were 0.738 for p53, 0.674 for Ki67, 0.638 for pTNM staging, and 0.587 for histological grade. Among these, p53 demonstrated the highest predictive efficacy. Conclusions:AI-assisted interpretation of P53 and Ki67 indices improves test result repeatability. With critical values of 62% and 20%, high P53 and Ki67 expression indicates poor prognosis, while high P53 expression is an independent risk factor for lower OS and DFS, serving as a reference for postoperative adjuvant therapy screening.

AIM To investigate the protective effect of Sanfeng Tongqiao Dropping Pills against house dust mite(HDM)-induced allergic asthma in mice.METHODS Compared to the intact BALB/c mice in the blank control group,the BALB/c mice randomly assigned into the model group,the dexamethasone group(0.67 mg/kg),and the low-dose,medium-dose,and high-dose Sanfeng Tongqiao Dropping Pills groups(15,30 and 60 mg/kg),were induced into acute allergic asthma models via weekly intraperitoneal sensitization with 0.1 mL HDM solution(0.5 mg/mL)for three weeks followed by three consecutive daily intranasal challenges with 10 μL HDM solution(2.5 mg/mL)starting in the third week.The drug administered continuously 7 days after the last excitation.The mice had their airway reactive Penh value detected,their pulmonary pathological changes observed by HE staining,their blood eosinophils(EOS)counted,their Th2 cytokines in lung tissue and serum IgE levels detected by ELISA,and their number of peripheral blood mononuclear cells(PBMC)and pulmonary Th2 cells detected by flow cytometry.Chronic allergic asthma was induced in grouped BALB/c mice through repeated intranasal challenges with 10 μL HDM solution(2.5 mg/mL)administered five times weekly for five consecutive weeks.Drug treatment continued for 14 days following the final challenge.After the final treatment,the mice had their pulmonary pathological changes observed by HE staining,and their levels of Th2 cytokines in B ALF and lung tissue and serum IgE detected by ELISA.RESULTS Compared to the blank control group,the acute allergic asthma model group exhibited increases in Penh value,EOS count and IgE level in serum,IL-4 and IL-5 levels in lung tissue(P＜0.01);obvious pulmonary inflammatory cells infiltration,and thickened airway wall;and increase in pulmonary number of Th2 cells(P＜0.01).Compared to the model group,the groups intervened with Sanfeng Tongqiao Dropping Pills demonstrated decreased Penh value,serum EOS count,IgE level and IL-5 level in lung tissue(P＜0.05,P＜0.01);reduced pulmonary inflammatory infiltration and alleviated airway wall thickening;and decreased number of pulmonary Th2 cells.Compared to the blank group,the chronic allergic asthma model group showed obvious pulmonary inflammatory infiltration and airway wall thickening;and increased EOS count and IgE level in serum,IL-4 and IL-13 in lung tissue and IL-14 in BALF(P＜0.05,P＜0.01).Compared to the model group,the groups intervened with either medium-dose or high-dose Sanfeng Tongqiao Dropping Pills demonstrated reduced pulmonary inflammatory infiltration;and decreased serum EOS count,IgE level,IL-13 in lung tissue and IL-14 in BALF(P＜0.05,P＜0.01).CONCLUSION Sanfeng Tongqiao Dropping Pills reduce Th2 cells in peripheral blood and lung tissue,suppress type 2 inflammation,and thereby alleviate allergic asthma.

Objective:To investigate the effects of toosendanin(TSN)on the proliferation,apoptosis,migration and invasion of esophageal squamous cell carcinoma(ESCC)KYSE150 cells,and to elucidate its underlying molecular mechanisms.Methods:CCK-8 assay,colony formation assay,and EdU assay were used to assess the effects of varying TSN concentrations(0.062 5,0.125,and 0.25 μmol/L)on KYSE150 cell proliferation.The impacts of TSN on the apoptosis,migration,and invasion of KYSE150 cells were evaluated using flow cytometry,wound healing assay,and Transwell chamber assay,respectively.The expression of hypoxia-inducible factor 1 alpha(HIF1A)in esophageal cancer tissues was analyzed using the GEPIA database.qPCR was used to detect the expression level of HIF1A mRNA in human esophageal epithelial Het-1A and KYSE150 cells,and in TSN-treated KYSE150 cells.Western blot(WB)was performed to detect the effects of TSN on the upstream signaling pathway AKT/mTOR of HIF1A and the expression of downstream proteins related to cell migration,invasion,and apoptosis.Results:TSN of varying concentrations significantly inhibited proliferation,migration,and invasion of KYSE150 cells and promoted apoptosis in a dose-dependent manner(P<0.05 or P<0.01).HIF1A mRNA was highly expressed in KYSE150 cells,and its expression was significantly downregulated after TSN treatment(P<0.05 or P<0.01).TSN markedly downregulated the expression of HIF1A and key upstream signaling proteins p-AKT and p-mTOR.In addition,TSN significantly suppressed the expression of downstream proteins associated with cell migration,invasion,and apoptosis,including N-cadherin,vimentin,Bcl-2,and caspase-3,while upregulating the expression of E-cadherin(P<0.05 or P<0.01).Conclusion:TSN inhibits the proliferation,migration,and invasion,and induces apoptosis in ESCC KYSE150 cells by down-regulating HIF1A expression through suppression of the AKT/mTOR signaling pathway.

Approximately 70% epilepsy may be associated with genetic etiology. To date, more than 2 900 genes related to epilepsy have been reported, and genotype-phenotype association in epilepsy has received increasing attention. Explaining how mutations in the same gene can lead to different diseases or phenotypes remains challenging. Sub-molecular mechanisms, including functional structural domains, amino acid substitutions, isoforms, and monoallelic/biallelic mutations, provide new perspectives for deciphering genotype-phenotype association in epilepsy. This review summarizes the role of sub-molecular mechanisms in genotype-phenotype association in epilepsy, to provide new strategies for clinical diagnosis and precise treatment of epilepsy.

Objective:To study the effect and mechanism of ganoderma lucidum polysaccharide peptide(GLPP)on renal anti oxidative stress and immune inflammation in diabetes nephropathy mice.Methods:The C57 male mice model of diabetes nephropathy was established by streptozotocin combined with high glucose and high-fat diet.Sixty diabetes nephropathy mice were divided into model group,losartan group,GLPP group(low,medium and high dose groups),GLPP high-dose+losartan group,with 10 mice in each group,10 mice fed with normal diet as the blank group.The losartan group was given 10 mg/kg losartan by gavage,and GLPP low,medium and high dose groups was given 50,100,and 200 mg/kg GLPP by gavage,while the GLPP high-dose+losartan group were given 200 mg/kg GLPP+10 mg/kg losartan by gavage.The blank group and model group were given physiological saline by gavage.After gastric lavage,observe the diet,water intake,renal pathology,structure,and apoptosis of renal tubular epithelial cells in mice,and analyze the levels of blood biochemical indicators,immune inflammation,oxidative stress indicators,and expression of apoptosis/cycle regulatory proteins in mice.Results:Compared with the blank group,the model group showed an increase in blood biochemical indicators such as Scr,BUN,TC,TG and GSP(P<0.05),as well as inflammation indicators such as level of IL-6 and TNF-α、MCP-1 were decreased(P<0.05),the oxidative stress indicator MDA was increased,T-AOC,GSH-PX,SOD were decreased(P<0.05),the apoptosis rate of renal tubular epithelial cells were increased(P<0.05),the expression levels of Bax,Caspase-3,P53,P21 were all increased,and the expression levels of Bcl-2 and Cyclin D1 were decreased(P<0.05).Compared with the model group,the losartan group,GLPP dose groups,GLPP high-dose+losartan group Scr,BUN,TC,TG,GSP,IL-6,TNF-α,MCP-1,MDA levels,apoptosis rate of renal tubular epithelial cells,Bax,Caspase-3,P53,P21 expression levels were all reduced,while T-AOC,SOD,GSH-PX levels,Bcl-2,and Cyclin D1 expression levels were all increased.Renal pathological changes were improved,and mitochondrial swelling was reduced.The GLPP high-dose+losartan group showed the most significant improvement(P<0.05).Conclusion:GLPP can reverse the renal injury in diabetes nephropathy mice,which may be related to the inhibition of apoptosis of renal tubular epithelial cells by alleviating renal oxidative stress and immune inflammatory damage.