Mulberry leaf, as a traditional Chinese medicinal plant, has been utilized in the treatment of various diseases, including diabetes, cardiovascular diseases, inflammatory disorders, and liver diseases. However, the mechanisms underlying its therapeutic effects on non-alcoholic fatty liver disease (NAFLD) remain unclear. Therefore, this study aims to investigate the potential mechanisms of mulberry leaf extract (MLE) in the treatment of NAFLD. The chemical composition of MLE was analyzed using ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS). The NAFLD mice model was induced by a high-fat, high-fructose, and high-cholesterol (HFFC) diet, followed by intervention with MLE. The results indicated that the administration of MLE notably reduced the obesity (p < 0.05), oxidative stress (p < 0.05), inflammation (p < 0.05), and ECM deposition (p < 0.05) induced by the HFFC diet, restored the parameters of liver function, and attenuated the pathological changes. Utilizing a combination of integrated liver non-targeted metabolomics, network pharmacology, and transcriptomic approaches, we deciphered the molecular mechanisms by which MLE exerted its therapeutic effects in the treatment of NAFLD. In detail, our findings revealed that MLE suppressed the TGFβ1/Smad3 and NF-κB signaling pathways to ameliorate fibrosis and inflammation. This study provided novel insights into the correlation between MLE and NAFLD progression, offering a scientific foundation for the prospective use of MLE in the treatment of NAFLD.

BACKGROUND:Dysregulated lactate metabolism and endoplasmic reticulum (ER) stress contribute to sepsis-associated acute kidney injury (AKI). We tested whether sodium lactate mitigates LPS-induced AKI in association with reduced CHOP signaling. METHODS:LPS-induced AKI was established in mice and modeled in HK-2 cells. NALA was administered in vivo and in vitro. Renal injury was assessed by histology and renal function (serum creatinine, blood urea nitrogen). Inflammatory and apoptotic signaling (IL-6, IL-1β, TNF-α; Bcl-2, Bax, cleaved caspase-3) and ER-stress markers (CHOP) were quantified by western blotting and RT-qPCR. The glycolytic enzymes LDHA and PKM2 were measured to explore effects on lactate-related metabolism. Group comparisons used standard parametric/non-parametric tests and one-way ANOVA with multiple comparisons. RESULTS:In mice, NALA attenuated tubular injury and lowered serum creatinine and urea nitrogen compared with LPS alone. Renal expression of IL-6, IL-1β and TNF-α decreased with NALA, accompanied by increased Bcl-2 and reduced Bax and cleaved caspase-3. NALA downregulated CHOP in renal tissue. In HK-2 cells, NALA similarly blunted LPS-induced inflammatory cytokines and apoptosis-related changes and reduced CHOP expression. Across models, NALA decreased LDHA and PKM2 expression, indicating modulation of glycolysis-linked lactate metabolism. CONCLUSIONS:NALA mitigates LPS-induced AKI in vivo and in vitro, associated with suppression of CHOP expression, ER stress, dampening of inflammatory and apoptotic signaling, with concomitant effects on LDHA/PKM2. These findings support further evaluation of sodium lactate as a metabolism-informed intervention for sepsis-related AKI, including dose-response, time-course, and upstream UPR-branch analyses in extended preclinical studies.

Rationale:Doxorubicin (DOX) is a potent chemotherapeutic agent whose antitumor benefits are limited by a well-recognized, dose-dependent cardiotoxicity. While previous studies have implicated inflammatory pathways in DOX-induced cardiomyopathy (DIC), the role of CCR2 in this process remains incompletely defined. This study aims to investigate whether CCR2 deficiency confers cardioprotection against DIC and to uncover the molecular mechanisms involved. Methods:CCR2 knockout (CCR2⁻/⁻ ) mouse was subjected to both acute and chronic DIC models. Bone marrow transplantation was used to establish the functional contribution of CCR2-deficient macrophages. Autophagic flux was evaluated using complementary approaches, including a tandem mRFP-GFP-LC3 reporter, western blotting, immunofluorescence, and transmission electron microscopy. The mediator linking CCR2-deficient macrophages to cardiomyocytes was identified by proteomics and validated using recombinant IL12B protein and a neutralizing antibody. Results:CCR2 deficiency substantially improved cardiac function, as evidenced by preserved left ventricular ejection fraction, fractional shortening and reduced serum cardiac injury markers. Mechanistic studies revealed that CCR2⁻/⁻ hearts exhibited enhanced autophagic flux, with increased LC3B lipidation, autophagosome formation, and clearance of damaged cellular components. Proteomic profiling of cardiac macrophages identified interleukin-12B (IL12B) significantly upregulated in CCR2⁻/⁻ mouse. Recombinant IL12B protein administration activated cardiomyocyte autophagy through PI3K/Akt/mTOR pathway inhibition and reproduced the cardioprotective effects in WT mouse. Conversely, IL12B neutralization completely abolished CCR2 deficiency-mediated protection. Conclusions:Our findings identify a novel CCR2-IL12B-autophagy axis that critically regulates DOX-induced cardiotoxicity. CCR2 deficiency promotes IL12B secretion from cardiac macrophages, which directly activates protective autophagy in cardiomyocytes. These results establish CCR2 inhibition and IL12B supplementation as two promising therapeutic strategies to prevent chemotherapy-induced cardiomyopathy, providing a transformative approach to cardio-oncology.

The ATP-binding cassette (ABC) transporter superfamily is one of the largest membrane protein families existing widely in plants. ABC transporters are essential for pollen development in Arabidopsis thaliana. However, there are few reports on the function of the ABCB subfamily in plants. Here, 25 CaABCB genes were identified, which were unevenly distributed across 10 chromosomes. The cis-acting elements in the promoters of CaABCB genes are mainly related to hormone response, stress response and meristem expression. Among them, CaABCB20 exhibits robust expression in the anthers of pepper. CaABCB20 demonstrates high expression levels in fertile flower buds, whereas its expression is negligible in CMS lines. In addition, silencing CaABCB20 exhibited collapsed anthers, shriveled and deformed pollen, and reduced pollen viability and germination rates in pepper. These suggest that CaABCB20 plays a crucial role in anther and pollen development in pepper. This study provides new insights into the function of CaABCB transporters in male fertility regulation in pepper.

ETHNOPHARMACOLOGICAL RELEVANCE:Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent liver diseases worldwide, with an estimated global prevalence of 30 %. An imbalance in lipid metabolism leads to the accumulation of lipotoxic lipids, inducing cellular stress, activating the NLRP3 inflammasome, and triggering apoptotic cell death. This cascade stimulates inflammation, driving NAFLD progression. Morus nigra L. is the only black mulberry species native to China. In traditional Uygur medicine, its fruit is valued for its hepatoprotective and lipid-lowering effects. AIM OF THE STUDY:The mechanism by which mulberry extract (ME) alleviates NAFLD remains unclear. This study aimed to investigate the hepatoprotective and anti-inflammatory effects of ME. MATERIALS AND METHODS:Network pharmacology was employed to predict the active components of ME and their potential target genes. Liver function markers (ALT, AST) and lipid profiles (TG, TC) were assessed using commercial assay kits. The therapeutic mechanism of ME against NAFLD was elucidated through an integrated approach combining transcriptomic and metabolomic analyses in a mouse NAFLD model. RESULTS:UPLC-QTOF-MS analysis identified 131 active ingredients in ME. Network pharmacological analysis identified Akt1, Pparg, and Pparα as core targets. High-dose ME treatment markedly improved liver function, reducing ALT levels by 50 % and AST levels by 44 %, while also lowering hepatic TG by 22 % and TC by 15 %. Transcriptome analysis revealed that ME ameliorated NAFLD through AMPK/PPAR-γ/NF-κB axis. Metabolomic analysis demonstrated the involvement of unsaturated fatty acid and steroid hormone biosynthesis in NAFLD metabolism. CONCLUSIONS:Our study demonstrates that ME alleviates NAFLD progression by regulating the AMPK/PPAR-γ/NF-κB signaling axis. However, these findings are based on preclinical animal studies, and further investigation is required to determine the clinical applicability of these effects in human patients.

Liver fibrosis, characterized by excessive extracellular matrix (ECM) accumulation, poses a significant threat to human health. This study synthesized a novel anthraquinone derivative, Kanglexin (KLX), and evaluated its protective effects against liver fibrosis while elucidating the underlying molecular mechanisms. Hepatic fibrosis was induced in mice via intraperitoneal carbon tetrachloride (CCl₄) injection, and an in vitro model of activated hepatic stellate cells (HSCs) was established using transforming growth factor-beta (TGF-β) stimulation. Transcriptomic analysis was employed to investigate KLX's mechanisms. In vivo, KLX significantly attenuated CCl₄-induced increases in serum fibronectin (FN), hyaluronic acid (HA), laminin (LN), collagen type IV (Col-IV), and TGF-β levels, alongside reducing collagen fiber deposition. KLX also reversed the CCl₄-induced imbalance in hepatic superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels. Transcriptomics revealed that retinol metabolism, glutathione metabolism, and cellular migration pathways are potentially pivotal for KLX's antifibrotic action. KLX mitigated CCl₄-induced upregulation of phosphoenolpyruvate carboxykinase 1 (PCK1) protein and downregulation of the cystine/glutamate antiporter (xCT), thereby modulating glutathione metabolism. In vitro, KLX suppressed the TGF-β/SMADs signaling pathway and regulated the expression of tissue inhibitors of metalloproteinases/matrix metalloproteinases (TIMPs/MMPs) to enhance ECM degradation balance. Furthermore, KLX downregulated cyclin-dependent kinase inhibitor 1 (Cyclin D1) and cyclin-dependent kinase 2 (CDK2) expression, inhibiting activated HSC proliferation. KLX also improved glutathione metabolism by modulating the expression of PCK1, xCT, and glutathione peroxidase 4 (GPX4)-related proteins. These findings demonstrate that KLX exerts potent antifibrotic effects by regulating glutathione metabolism and promoting ECM degradation, suggesting its potential as a therapeutic candidate for liver fibrosis.

The metabolic dependence of acute myeloid leukemia (AML) cells on mitochondrial oxidative phosphorylation (OXPHOS) has become a cutting-edge area in cancer energy metabolism research, playing a pivotal role in cell survival and drug resistance. Consequently, targeted inhibition of human mitochondrial RNA polymerase (POLRMT) to block mitochondrial gene expression emerges as a novel potential strategy for treating AML through OXPHOS modulation. In this study, based on the previously reported crystal structure of the POLRMT inhibitor IMT1B, we employed a scaffold hopping strategy to design and synthesize a series of derivatives featuring additional hydrophobic occupying groups. A new potent POLRMT inhibitor (10a) was discovered, which displayed potent antiproliferative activity and could disrupt mitochondrial function and induce apoptosis in MOLM-13 cells. Together, these results demonstrate that 10a is a new POLRMT inhibitor, which may provide a candidate lead for AML treatment.

BACKGROUND:Renal fibrosis (RF), a major contributor to the progression of chronic kidney disease (CKD), is an important therapeutic target. Eucalyptus oil (EO), a volatile extract derived from traditional Chinese herbal medicine with known anti-inflammatory and antioxidant properties, has shown potential in CKD treatment. However, its efficacy and mechanisms in preventing kidney injury induced by unilateral ureteral obstruction (UUO) remain unclear. PURPOSE:This study aimed to evaluate the protective effects of EO against renal injury in UUO rats and to investigate its underlying mechanisms of action. METHODS:A UUO-induced rat model of RF was established to assess the antifibrotic effects of EO. Integrated multi-omics approaches, including genomic and metabolomic analyses, along with molecular docking and experimental validation using Western blot and qPCR, were employed to systematically elucidate the molecular mechanisms and pharmacodynamic basis of EO in alleviating RF. RESULTS:EO significantly reduced RF in the UUO model by concurrently inhibiting the transforming growth factor-beta 1 (TGF-β1)/Smad3 signaling pathway and the tryptophan metabolism-aryl hydrocarbon receptor (AhR) axis. Specifically, EO suppressed Smad3 phosphorylation, fibroblast activation, and extracellular matrix (ECM) accumulation. It also inhibited AhR nuclear translocation and reduced the expression of cytochrome P450 1A1 (Cyp1A1), cytochrome P450 1B1 (Cyp1B1), and aryl hydrocarbon receptor nuclear translocator (ARNT). These molecular effects were associated with improvements in renal function indicators, including reductions in serum creatinine (SCR), blood urea nitrogen (BUN), and kidney injury molecule-1 (KIM-1). EO also mitigated histological damage and decreased oxidative stress markers-malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH)-as well as inflammatory mediators-monocyte chemoattractant protein-1 (MCP-1), interleukin-1 beta (IL-1β), and tumor necrosis factor-alpha (TNF-α). These findings highlight the multitarget antifibrotic potential of EO. CONCLUSION:EO suppresses renal fibrosis by inhibiting both the TGF-β1/Smad3 signaling pathway and the tryptophan metabolism-AhR pathway, thereby reducing abnormal ECM accumulation.

Idiopathic pulmonary fibrosis is a progressive, highly lethal disease with limited treatment options. It is characterized by fibroblast-to-myofibroblast transformation, excessive ECM proliferation and collagen deposition, leading to the destruction of normal lung architecture and function. As a constituent of Rhodiola rosea L., rosiridin is a monomer with significant structural compatibility, conferring strong therapeutic potential. This bioactive compound mitigates oxidative stress-driven pathology and reverses its resultant damage in various diseases. However, its potential protective effects against bleomycin-induced IPF and the underlying mechanisms remain unclear. This study aimed to investigate the role and mechanism of rosiridin in IPF. Rosiridin attenuated TGF-β1-induced oxidative stress and inflammatory responses in lung epithelial cells and suppressed apoptosis associated with pulmonary fibrosis. Hematoxylin and eosin (HE) staining and Masson's trichrome staining showed that rosiridin improved pathological lung changes, reduced oxidative stress, and alleviated pulmonary fibrosis in a dose-dependent manner. Transcriptomic analysis revealed that rosiridin inhibited JAK protein activation, reduced the transformation of fibroblasts into myofibroblasts, and suppressed the secretion of proinflammatory and profibrotic cytokines. These findings suggest that rosiridin mitigates pulmonary fibrosis through modulation of the STAT3/NF-κB/SMAD3 signaling pathways. Rosiridin may represent a promising therapeutic candidate for the treatment of IPF.

Shenhua Tablet (SHT), a Chinese herbal medicine comprising seven crude drugs, is utilized in the treatment of immunoglobulin A nephropathy (IgAN). However, due to its complex composition, the chemical constituents of SHT in vitro are still incompletely known, which has restricted the comprehensive development and utilization of SHT in clinical practice. In the present study based on ultra-high performance liquid chromatography-quadrupole-orbitrap-linear ion trap mass spectrometry (UHPLC-Q-Orbitrap-LTQ-MS) in data dependent acquisition mode, combining the accurate mass and structural information, the profiling and characterization of chemical constituents in SHT were carried out. The automated spectral matching (of experimental MS2 spectra against library spectra of mzCloud) method with a high mass accuracy (within 5 ppm) was used for the rapid identification of compounds. A total of 183 compounds, consisting of 64 flavonoids, 52 terpenoids, 37 organic acids, 6 phenylpropanoids, 5 phenols, and 19 other phytochemicals, were successfully characterized. In addition, the fragmentation pathways and characteristic fragments of some representative compounds were elucidated. The results offered clear insights into its chemical profile, thereby facilitating quality control and advancing pharmacological research.

To address the challenges of vehicle target detection in aerial images from Unmanned Aerial Vehicle (UAV) perspectives, this paper proposes a novel vehicle detection model named UAV-YOLO, based on the YOLOv7 object detection framework. First, Omni-dimensional Dynamic Convolution (ODConv) is introduced into the backbone of the feature extraction network to enrich the acquisition of small target information, enhancing the network's capability to extract features of small objects. Second, the Mixed Local Channel Attention (MLCA) module is added to the ELAN and feature pyramid structures within the backbone feature extraction module to integrate both local and global information, further improving the model's perception and information fusion for small targets. Lastly, a joint loss function, Normalized Wasserstein Complete IoU Loss (NWC-IoU Loss), is designed to enhance the model's detection performance and stability for small targets. Experimental results show that the improved detection algorithm increases the mean Average Precision (mAP@0.5) by 4.8%, reduces the FLOPs by 27.3%, and achieves a detection speed of 62.2 FPS, meeting real-time requirements. The proposed method demonstrates superior detection performance in various complex scenarios of the VisDrone2019 dataset. The UAV -YOLO model exhibits excellent performance in vehicle target detection in aerial images from UAV perspectives.

With the increasing incidence of chronic kidney disease (CKD), the development of safe and effective anti-renal fibrosis drugs is particularly urgent. Recently, Baicalin has been considered to have a renal protective effect, but its bioavailability is too low. Therefore, we synthesized baicalin-2-ethoxyethyl ester (BAE) by esterification of baicalin. We hope that this experiment will demonstrate the anti-renal fibrosis effect of BAE and explain its molecular mechanism. In this study, the chronic kidney injury model of SD rats was established by 5/6 nephrectomy, and BAE was given for 28 days. The results showed that after BAE treatment, the serum creatinine and urea nitrogen levels decreased significantly, and the pathological changes in kidneys were improved. In addition, RNA-seq analysis showed that the mechanism of BAE in relieving renal fibrosis was related to the ECM receptor, PI3K/AKT signaling pathway, and inflammatory reaction. The western blotting analysis confirmed that BAE could inhibit the expression of a-SMA, TGF-beta 1, p-PI3K, p-AKT, p-IxBa, and NF-xB p65. We found that BAE can inhibit the inflammatory reaction and promote the degradation of the extracellular matrix by inhibiting the activation of the PI3K/AKT/NF-xB pathway, thus alleviating the symptoms of renal fibrosis in 5/6Nx rats, which revealed BAE was a potential compound to relieve renal fibrosis effect.

With the development of automation technology, seven degrees of freedom robotic arms are widely used in industry, but the complex kinematic characteristics make path planning a challenge. In this paper, an improved RRT algorithm is proposed for seven-degrees-of-freedom robotic arm path planning to solve the high-dimensional complex constraint problem. Although the traditional RRT algorithm is efficient and adaptable, it suffers from non-optimal paths, redundancy and litter problems. For this reason, this paper introduces a goal strategy and heuristic term to reduce redundant nodes and improve the convergence speed by guiding the tree expansion with goal bias and stochastic probability. Meanwhile, collision detection and fifth-degree polynomial interpolation are used to ensure path safety and motion smoothing.

Drug nephrotoxicity has high fatality rates and complications. To study this conditional, traditionally, Gentamicin (GM) is used to induce acute injury and establish a nephrotic syndrome model. Baicalin, a flavonoid derived from baicalin with potent anti-inflammatory and antioxidant activity, has been used to treat various inflammatory diseases. This study aims to investigate the process of baicalin-2-ethoxyethyl ester (BAE) synthesis and its therapeutic effect on GM-induced acute kidney injury (AKI). Briefly, baicalin was processed by various reactions to yield BAE. A GM-induced AKI model was established for in vivo evaluation of the protective effect and mechanism of BAE. The results indicated that BAE reduced serum creatinine and urea nitrogen levels and improved pathological alterations, inflammatory responses, and oxidative stress in renal tissues. Furthermore, it was revealed that BAE might exert anti-inflammatory and anti-oxidative responses during AKI via the NF-κB signaling pathway regulation. The findings imply that BAE has a protective impact on the kidneys and might serve as a potent medicine for treating renal damage.

With the increasing incidence of chronic kidney disease (CKD), the development of safe and effective anti-renal fibrosis drugs is particularly urgent. Recently, Baicalin has been considered to have a renal protective effect, but its bioavailability is too low. Therefore, we synthesized baicalin-2-ethoxyethyl ester (BAE) by esterification of baicalin. We hope that this experiment will demonstrate the anti-renal fibrosis effect of BAE and explain its molecular mechanism. In this study, the chronic kidney injury model of SD rats was established by 5/6 nephrectomy, and BAE was given for 28 days. The results showed that after BAE treatment, the serum creatinine and urea nitrogen levels decreased significantly, and the pathological changes in kidneys were improved. In addition, RNA-seq analysis showed that the mechanism of BAE in relieving renal fibrosis was related to the ECM receptor, PI3K/AKT signaling pathway, and inflammatory reaction. The western blotting analysis confirmed that BAE could inhibit the expression of α-SMA, TGF-β1, p-PI3K, p-AKT, p-IκBα, and NF-κB p65. We found that BAE can inhibit the inflammatory reaction and promote the degradation of the extracellular matrix by inhibiting the activation of the PI3K/AKT/NF-κB pathway, thus alleviating the symptoms of renal fibrosis in 5/6Nx rats, which revealed BAE was a potential compound to relieve renal fibrosis effect.

Acute lung injury (ALI) is a serious inflammatory disease with high morbidity and mortality. Rosavin is an anti-inflammatory and antioxidant phenylpropanoid and glucoside, which is isolated from Rhodiola rosea L. However, its potential molecular mechanisms and whether it has protective effects against lipopolysaccharide (LPS)-induced ALI remain to be elucidated. To assess the in vitro anti-inflammatory effects and anti-lung injury activity of rosavin, RAW264.7 and A549 cells were stimulated using 1 μg/mL LPS. Rosavin attenuated LPS-induced activation of the TLR-4/NF-κB signaling pathway in RAW264.7 cells and inhibited LPS-induced release of inflammatory factors in A549 cells. A mouse model of acute lung injury was constructed by intraperitoneal injection of 5 mg/kg LPS to observe the therapeutic effect of rosavin. Transcriptomics analysis and Western blot assays were utilized to verify the molecular mechanism, rosavin (20, 40, and 80 mg/kg) dose-dependently ameliorated histopathological alterations, reduced the levels of inflammatory factors, and inhibited the TLR-4/NF-κB/MAPK signaling pathway and apoptosis activation. Rosavin is a promising therapeutic candidate for acute lung injury by inhibiting the TLR-4/NF-κB/MAPK pathway.

目的 研究合成出的嘧啶甲酸乙酯类化合物的1 H-NMR图谱,确证其结构并分析图谱规律;方法 经 Biginelli缩合反应所得六种化合物,测定的1H-NMR图谱分别与计算机分析软件模拟结果及文献值相对照,比较各质子在图谱中的化学位移;结果 丰富了的波谱数据,找出并检定了相关化合物1H-NMR 图谱出峰顺序和规律,并定性确证了化合物;结论 合成工艺可行且结构为预设化合物.

Acute lung injury (ALI) is a common respiratory disease in clinics, which is characterized by alveolar-capillary membrane loss, plasma protein leakage, pulmonary edema, massive neutrophil infiltration, and the release of proinflammatory cytokines and mediators. Rhodiola rosea L. an adaptogenic plant rich in phenylethanoloids, phenylpropanoids, monoterpenes, has anti-inflammatory and antioxidant effects. We hope to verify the relieving effect of total glycosides of Rhodiola rosea L. (RTG) on ALI in mice and clarify its mechanism through this study. In this study, we identified the effect and mechanism of RTG on ALI through LPS-induced ALI mice. After RTG treatment, the pathological structure of lung tissue in ALI mice induced by LPS was significantly improved, and the infiltration of inflammatory cells was reduced. In addition, RTG reduced the production of IL-6, IL-1β, and TNF-α in the serum of ALI mice and reduced the content or activity of MPO, T-SOD, GSH, and MDA in lung tissue. RNAseq analysis showed that RTG ameliorated LPS-induced ALI through anti-inflammatory, reduced immune response, and anti-apoptotic activities. The western blotting analysis confirmed that RTG could down-regulate the expression levels of TLR4, MyD88, NF-κB p65, and p-IκBα/IκBα. These results suggest that RTG can attenuate LPS-induced ALI through antioxidants and inhibition of the TLR4/NF-κB pathway.

目的 探讨山楂叶提取物对庆大霉素致急性肾损伤(AKI)大鼠的保护作用及机制.方法 大鼠连续 7 d腹腔注射 100 mg·kg-1庆大霉素,诱导急性肾损伤的发生.通过测定血清BUN、SCR和尿液NAG、LZM 含量,检测模型是否成功建立.将急性肾损伤大鼠随机分为模型组,山楂叶提取物低剂量组,山楂叶提取物中剂量组,山楂叶提取物高剂量组及阳性药组,口服给药 14 d.血清用于检测肾功能指标;肾组织进行苏木精-伊红(HE)染色,肾组织匀浆用以检测生化指标及炎症因子含量、MAPK信号通路的相关蛋白表达水平.结果 大鼠连续 7 d腹腔注射 100 mg·kg-1庆大霉素可成功建立急性肾损伤模型.山楂叶提取物能缓解庆大霉素引起的肾组织病理学改变,降低肾体指数和血清 BUN、SCR含量,降低肾组织 NO、MDA、NOS含量,增加 SOD和 GSH-PX含量,降低炎症因子 IL-1β、IL-6、TNF-α和 KIM-1 的表达,抑制肾组织中 P-p38 MAPK、P-ERK1/2、P-JNK蛋白的表达.结论 山楂叶提取物对庆大霉素致 AKI大鼠有保护作用,可能是通过抑制 MAPK信号通路表达,从而减轻炎症因子释放,改善肾损伤,起到保护肾功能作用.