Cervicovaginal microbiota: a promising direction for prevention and treatment in cervical cancer.

Cervical cancer is a common malignancy in women, with high incidence rate and mortality. Persistent infection of high-risk human papillomavirus (HPV) is the most important risk factor for cervical cancer and precancerous lesions. Cervicovaginal microbiota (CVM) plays an essential role in the defense of HPV infections and prevention of subsequent lesions. Dominance of Lactobacillus is the key of CVM homeostasis, which can be regulated by host, exogenous and endogenous factors. Dysbiosis of CVM, including altered microbial, metabolic, and immune signatures, can contribute to persist HPV infection, leading to cervical cancer. However, there is no evidence of the causality between CVM and cervical cancer, and the underlying mechanism remains unexplored. Considering the close correlation between CVM dysbiosis and persistent HPV infection, this review will overview CVM, its role in cervical cancer development and related mechanisms, and the prospects for therapeutic applications.

Hemostatic and Ultrasound-Controlled Bactericidal Silk Fibroin Hydrogel via Integrating a Perfluorocarbon Nanoemulsion.

Excessive blood loss and infections are the prominent risks accounting for mortality and disability associated with acute wounds. Consequently, wound dressings should encompass adequate adhesive, hemostatic, and bactericidal attributes, yet their development remains challenging. This investigation presented the benefits of incorporating a perfluorocarbon nanoemulsion (PPP NE) into a silk-fibroin (SF)-based hydrogel. By stimulating the ß-sheet conformation of the SF chains, PPP NEs drastically shortened the gelation time while augmenting the elasticity, mechanical stability, and viscosity of the hydrogel. Furthermore, the integration of PPP NEs improved hemostatic competence by boosting the affinity between cells and biomacromolecules. It also endowed the hydrogel with ultrasound-controlled bactericidal ability through the inducement of inner cavitation by perfluorocarbon and reactive oxygen species (ROS) generated by the sonosensitizer protoporphyrin. Ultimately, we employed a laparotomy bleeding model and a Staphylococcus aureus-infected trauma wound to demonstrate the first-aid efficacy. Thus, our research suggested an emulsion-incorporating strategy for managing emergency wounds.

Potential Cause-and-Effect Relationship between Gut Microbiota and Childhood Neuroblastoma: A Mendelian Randomization Analysis.

OBJECTIVES: To analyze the potential causal-effect of gut microbiota (GM) on neuroblastoma (NB) risk using a Mendelian randomization (MR) study. METHODS: A two-sample MR study was conducted using summary statistics of the GM from the largest available meta-analysis of genome-wide association studies conducted by the MiBioGen consortium. Pooled statistics for childhood NB were obtained from the IEU Consortium release data (1627 cases and 3254 controls). Inverse variance-weighted, weighted median, MR-Egger, and weighted mod were used to examine the causal relationship between GM and childhood NB. Single-nucleotide polymorphism (SNP) genes of positive GM were extracted using the PLINK program, and correlations between key SNP genes and tumor-regulated genes were analyzed. Functional enrichment analysis and transcription factor prediction were performed. RESULTS: Inverse variance weighted (IVW) results indicated that Erysipelotrichia exerted a protective effect against childhood NB (odds ratio = 0.371, 95% Confidence interval: 0.173 - 0.795, P = 0.011) and that Oscillospira exerted a risk effect against childhood NB (odds ratio = 2.378, 95% Confidence interval: 1.121 - 5.043, P = 0.024), indicating the association of GM with childhood NB. Further screening analysis using the IVW test revealed a reliable causal relationship between Erysipelotrichia and NB. Two SNP genes (MUC4 and PELI2) of Erysipelotrichia were extracted and analyzed. Both key genes were significantly associated with tumor-regulated genes, enriched in several pathways associated with tumor progression, and correlated with several upstream transcription factors. CONCLUSIONS: It was observed that Erysipelotrichia is causally associated with NB using a two-sample MR study. Furthermore, the discovery of two SNP genes, MUC4 and PELI2, provides potential targets for the diagnosis and treatment of NB.

Overexpression of Nrf2 reverses ferroptosis induced by Arenobufagin in gastric cancer.

Arenobufagin (ArBu) is a natural monomer extracted and isolated from the secretion of the Chinese toad, also known as toad venom. This compound exerts anti-tumor effects by promoting apoptosis in tumor cells, inhibiting tumor angiogenesis, and preventing the invasion and migration of tumor cells. However, their impact on ferroptosis in tumor cells has yet to be fully confirmed. In this study, we established a subcutaneous transplant tumor model in nude mice to investigate the inhibitory effect of ArBu on gastric cancer cells (MGC-803) and the safety of drug delivery. in vitro experiments, we screened the most sensitive cancer cell lines using the MTT method and determined the response of ArBu to cell death. Use flow cytometry to measure cytoplasmic and lipid reactive oxygen species (ROS) levels. Determine the expression levels of ferritin-related proteins through Western blot experiments. In addition, a MGC-803 cell model overexpressing Nrf2 was created using lentiviral transfection to investigate the role of ArBu in inducing ferroptosis in cancer cells. Our research findings indicate that ArBu inhibits the proliferation of MGC-803 cells and is linked to ferroptosis. In summary, our research findings indicate that ArBu is a potential anti-gastric cancer drug that can induce ferroptosis in human cancer cells through the Nrf2/SLC7A11/GPX4 pathway.

Paris polyphylla saponins II inhibits invasive, migration and epithelial-mesenchymal transition of melanoma cells through activation of autophagy.

Malignant melanoma is a kind of malignant tumor derived from normal epidermal melanocytes or original nevus cells. It has a high degree of malignancy, rapid progress, dangerous condition, and poor prognosis. In recent years, the innovation of traditional Chinese medicine has broadened the scope and effect of tumor treatment. It is a hotspot and breakthrough to find new anti-tumor invasion and migration drugs from natural plants or traditional Chinese medicine. This study explored the role of PPII in promoting autophagy to inhibit EMT of melanoma cells, the role of the PI3K/Akt signaling pathway in the invasion and migration of melanoma cells induced by PPII. We found that PPII effectively inhibited the proliferation, invasion and migration of melanoma B16 and B16F10 in vitro, and induced autophagy. We also established the xenograft tumor and metastatic tumor model of C57BL/6 mice with B16F10 cells. Results showed that PPII effectively inhibited the growth of transplanted tumors, induced autophagy and inhibited the expression level of EMT related protein; Metastasis experiment showed that PPII inhibited the invasion and migration of B16F10, the effect of inhibiting lung metastasis is the most significant. Further mechanism studies showed that the inhibition of PPII on melanoma invasion and migration is related to its induction of autophagy and then inhibition of EMT.

miR-26a-5p restoration via EZH2 silencing blocks the IL-6/STAT3 axis to repress the growth of prostate cancer.

BACKGROUND: Interleukin-6 (IL-6) is involved in the activation of several oncogenic pathways in prostate cancer. However, its upstream trans-signaling pathway remains largely unknown. This work proposes a mechanistic explanation of IL-6's upstream effectors in prostate carcinogenesis. RESEARCH DESIGN & METHODS: Samples were harvested to validate the expression of EZH2, miR-26a-5p, and IL-6. Moreover, the protein and its phosphorylation of STAT3 (signal transducer and transcription activator 3) were assessed in prostate cancer cells. We explored the effects of these effectors on malignant phenotypes in vitro and tumor growth in vivo using functional assays. Bioinformatics analysis, dual-luciferase reporter gene assays, and chromatin immunoprecipitation (ChIP) assays were used to determine their binding relationships. RESULTS: Overexpression of EZH2 and IL-6, and under expression of miR-26a-5p was observed in prostate cancer. Silencing IL-6 repressed STAT3 to suppress the malignant phenotypes of prostate cancer cells. Mechanistically, EZH2 inhibited miR-26a-5p expression by promoting H3K27 histone methylation, and miR-26a-5p restricted the malignant phenotypes of prostate cancer by targeting IL-6. Ectopic EZH2 expression reduced xenograft growth by inhibiting miR-26a-5p and activating the IL-6/STAT3 axis. CONCLUSION: EZH2 May potentially be involved in regulating its expression by recruiting H3K27me3 to the miR-26a-5p promoter region, which could further impact the IL6/STAT3 pathway.

Exploration of the molecular mechanism of intercellular communication in paediatric neuroblastoma by single-cell sequencing.

Neuroblastoma (NB) is an embryonic tumour that originates in the sympathetic nervous system and occurs most often in infants and children under 2 years of age. Moreover, it is the most common extracranial solid tumour in children. Increasing studies suggest that intercellular communication within the tumour microenvironment is closely related to tumour development. This study aimed to construct a prognosis-related intercellular communication-associated genes model by single-cell sequencing and transcriptome sequencing to predict the prognosis of patients with NB for precise management. Single-cell data from patients with NB were downloaded from the gene expression omnibus database for comprehensive analysis. Furthermore, prognosis-related genes were screened in the TARGET database based on epithelial cell marker genes through a combination of Cox regression and Lasso regression analyses, using GSE62564 and GSE85047 for external validation. The patients' risk scores were calculated, followed by immune infiltration analysis, drug sensitivity analysis, and enrichment analysis of risk scores, which were conducted for the prognostic model. I used the Lasso regression feature selection algorithm to screen characteristic genes in NB and developed a 21-gene prognostic model. The risk scores were highly correlated with multiple immune cells and common anti-tumour drugs. Furthermore, the risk score was identified as an independent prognostic factor for NB. In this study, I constructed and validated a prognostic signature based on epithelial marker genes, which may provide useful information on the development and prognosis of NB.

Mechanism of Paris polyphylla saponin II inducing autophagic to inhibit angiogenesis of cervical cancer.

Paris polyphylla saponin II (PPII) has good biological activity in inhibiting tumor angiogenesis. However, the mechanism of its action is still unclear. This study first observed the inhibitory effect of PPII on cervical cancer cells (Hela) through the establishment of MTT and nude mouse subcutaneous transplantation tumor models. Afterwards, then, we collected Hela cell supernatant for culturing HUVEC cells and treated it with PPII. Observe the invasion, migration, and lumen formation ability of drugs through Transwell, cell scratch test, and angiogenesis experiment. MDC staining was used to observe positive staining in the perinuclear area, AO staining was used to observe acidic areas, and transmission electron microscopy staining was used to observe ultrastructure and autophagy. In addition, the effects of PPII on autophagy- and angiogenesis-related protein expression were detected by Western blotting and quantitative reverse transcriptase polymerase chain reaction. Finally, HUVECs were treated with autophagy inhibitors 3-MA, CQ, and PI3K inhibitor LY294002, respectively. The results showed that the autophagy level of cells treated with PPII was significantly increased. In addition, adding autophagy inhibitors can effectively inhibit angiogenesis in cervical cancer. Further research suggests that PPII induces autophagy in HUVEC cells by regulating the PI3K/AKT/mTOR signaling pathway, thereby affecting angiogenesis and inhibiting Hela cell proliferation, lumen formation, invasion, and migration.

Dedifferentiated Schwann cells promote perineural invasion mediated by the PACAP paracrine signalling in cervical cancer.

Perineural invasion (PNI) has emerged as a key pathological feature and be considered as a poor prognostic factor in cervical cancer. However, the underlying molecular mechanisms are largely unknown. Here, PNI status of 269 cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) samples were quantified by using whole-slide diagnostic images obtained from The Cancer Genome Atlas. Integrated analyses revealed that PNI was an indicative marker of poorer disease-free survival for CESC patients. Among the differentially expressed genes, ADCYAP1 were identified. Clinical specimens supported that high expression of PACAP (encoded by ADCYAP1) contributed to PNI in CESC. Mechanistically, PACAP, secreted from cervical cancer cells, reversed myelin differentiation of Schwann cells (SCs). Then, dedifferentiated SCs promoted PNI by producing chemokine FGF17 and by degrading extracellular matrix through secretion of Cathepsin S and MMP-12. In conclusion, this study identified PACAP was associated with PNI in cervical cancer and suggested that tumour-derived PACAP reversed myelin differentiation of SCs to aid PNI.

25-hydroxyvitamin D levels in children of different ages and with varying degrees of Helicobacter pylori infection and immunological features.

Background: Helicobacter pylori (HP) is a major cause of upper digestive tract diseases. However, the relationship between HP infection and 25-hydroxyvitamin D [25(OH)D] levels in children has not been fully elucidated. This study investigated the levels of 25(OH)D in children of different ages and with varying degrees of HP infection and immunological features as well as the correlations between 25(OH)D levels in children infected with HP and their ages and degrees of infection. Materials and methods: Ninety-four children who underwent upper digestive endoscopy were divided into an HP-positive group without peptic ulcers (Group A), an HP-positive group with peptic ulcers (Group B) and an HP-negative control group (Group C). The serum levels of 25(OH)D and immunoglobulin and the percentages of lymphocyte subsets were determined. HP colonization, the degree of inflammation, and the degree of activity were further evaluated by HE staining and immunohistochemical staining in gastric mucosal biopsy. Results: The 25(OH)D level of the HP-positive groups (50.93 ± 16.51 nmol/L) was significantly lower than that of the HP-negative group (62.89 ± 19.18 nmol/L). The 25(OH)D level of Group B (47.79 ± 14.79 nmol/L) was lower than that of Group A (51.53 ± 17.05 nmol/L) and was significantly lower than that of Group C (62.89 ± 19.18 nmol/L). The 25(OH)D level decreased with increasing age, and there was a significant difference between Group C subjects who were ≤5 years old and those who were aged 6-9 years and ≥10 years. The 25(OH)D level was negatively correlated with HP colonization (r = -0.411, P < 0.01) and the degree of inflammation (r = -0.456, P < 0.01). The percentages of lymphocyte subsets and immunoglobulin levels among Groups A, B and C were not significantly different. Conclusions: The 25(OH)D level was negatively correlated with HP colonization and the degree of inflammation. As the age of the children increased, the level of 25(OH)D decreased, and the susceptibility to HP infection increased.

Synchronous Hepatoblastoma and Neuroblastoma in Two Chinese Infants.

Background: Commonly, pediatric solid tumors occur independently. Only two patients with synchronous hepatoblastoma (HBL) and neuroblastoma (NBL) have been reported. Case reports: Two Chinese infants presented with abdominal mass at 10 and 8 months. Computed tomography (CT) scans in both revealed hepatic masses with additional mediastinal or adrenal masses. Pathology confirmed synchronous HBLs in the liver and NBLs in the mediastinum and adrenal. Next generation sequencing (NGS) found no remarkable germline mutations. Both patients received gross total resections with chemotherapy before or after surgery. They were followed up for 36 and 8 months, and recovered well. Conclusion: These two cases of synchronous HBL and NBL tumors lacked significant genetic alterations.

Recognizing pathology of renal tumor from macroscopic cross-section image by deep learning.

OBJECTIVES: This study aims to develop and evaluate the deep learning-based classification model for recognizing the pathology of renal tumor from macroscopic cross-section image. METHODS: A total of 467 pathology-confirmed patients who received radical nephrectomy or partial nephrectomy were retrospectively enrolled. The experiment of distinguishing malignant and benign renal tumor are conducted followed by performing the multi-subtypes classification models for recognizing four subtypes of benign tumor and four subtypes of malignant tumors, respectively. The classification models used the same backbone networks which are based on the convolutional neural network (CNN), including EfficientNet-B4, ResNet-18, and VGG-16. The performance of the classification models was evaluated by area under the receiver operating characteristic curve (AUC), sensitivity, specificity, and accuracy. Besides, we performed the quantitative comparison among these CNN models. RESULTS: For the model to differentiate the malignant tumor from the benign tumor, three CNN models all obtained relatively satisfactory performance and the highest AUC was achieved by the ResNet-18 model (AUC = 0.9226). There is not statistically significance between EfficientNet-B4 and ResNet-18 architectures and both of them are significantly statistically better than the VGG-16 model. The micro-averaged AUC, macro-averaged sensitivity, macro-averaged specificity, and micro-averaged accuracy for the VGG-16 model to distinguish the malignant tumor subtypes achieved 0.9398, 0.5774, 0.8660, and 0.7917, respectively. The performance of the EfficientNet-B4 is not better than that of VGG-16 in terms of micro-averaged AUC except for other metrics. For the models to recognize the benign tumor subtypes, the EfficientNet-B4 ranked the best performance, but had no significantly statistical difference with other two models with respect to micro-averaged AUC. CONCLUSIONS: The classification results were relatively satisfactory, which showed the potential for clinical application when analyzing the renal tumor macroscopic cross-section images. Automatically distinguishing the malignant tumor from benign tumor and identifying the subtypes pathology of renal tumor could make the patient-management process more efficient.

Bioengineering Liver Organoids for Diseases Modelling and Transplantation.

Organoids as three-dimension (3D) cellular organizations partially mimic the physiological functions and micro-architecture of native tissues and organs, holding great potential for clinical applications. Advances in the identification of essential factors including physical cues and biochemical signals for controlling organoid development have contributed to the success of growing liver organoids from liver tissue and stem/progenitor cells. However, to recapitulate the physiological properties and the architecture of a native liver, one has to generate liver organoids that contain all the major liver cell types in correct proportions and relative 3D locations as found in a native liver. Recent advances in stem-cell-, biomaterial- and engineering-based approaches have been incorporated into conventional organoid culture methods to facilitate the development of a more sophisticated liver organoid culture resembling a near to native mini-liver in a dish. However, a comprehensive review on the recent advancement in the bioengineering liver organoid is still lacking. Here, we review the current liver organoid systems, focusing on the construction of the liver organoid system with various cell sources, the roles of growth factors for engineering liver organoids, as well as the recent advances in the bioengineering liver organoid disease models and their biomedical applications.

Lipid Metabolism and Cancer.

Lipid metabolism is involved in the regulation of numerous cellular processes, such as cell growth, proliferation, differentiation, survival, apoptosis, inflammation, movement, membrane homeostasis, chemotherapy response, and drug resistance. Reprogramming of lipid metabolism is a typical feature of malignant tumors. In a variety of cancers, fat uptake, storage and fat production are up-regulated, which in turn promotes the rapid growth, invasion, and migration of tumors. This paper systematically summarizes the key signal transduction pathways and molecules of lipid metabolism regulating tumors, and the role of lipid metabolism in programmed cell death. In conclusion, understanding the potential molecular mechanism of lipid metabolism and the functions of different lipid molecules may facilitate elucidating the mechanisms underlying the occurrence of cancer in order to discover new potential targets for the development of effective antitumor drugs.

Esthetics Effect and the Modified Placement of Robotic-Assisted Single-Site Laparoscopic Gynecologic Surgery by Common Robotic Instruments and LAGIS Single-Site Port.

OBJECTIVES: The accuracy of robotic surgery has been recognized by many doctors, but traditional robotic surgery requires 4-5 puncture holes in the operating area. With the popularization and application of single port laparoscopic surgery, the aesthetic of abdominal incision of robotic surgery has been challenged. How to use the single-site platform to complete robot operation is a new field worthy of our exploration. Here we introduce a kind of technology innovation of robot-assisted single-site laparoscopic surgery through common robotic equipment and LAGIS single-site port. METHODS: From November 2018 to March 2019, 20 patients with cervical cancer or endometrial cancer admitted to the minimally invasive gynecological group were included. Single-hole robotic surgery was successfully performed in all 20 patients, with no additional assisted puncture and no conversion to laparotomy. The operation time of patients, intraoperative bleeding volume and hospitalization time were recorded and compared. Besides, the Intraoperative complications were observed and analyzed. RESULTS AND CONCLUSIONS: By comparison, we can find that the effect of this innovative single-hole robotic surgery is significantly better than that of traditional single-hole laparoscopy.

Mechanism of hydrogen on cervical cancer suppression revealed by high­throughput RNA sequencing.

Cervical cancer is considered one of the diseases with the highest mortality among women and with limited treatment options. Hydrogen (H2) inhalation has been reported to have a variety of tumor­suppressive effects, but the exact mechanism remains unclear. In the present study, HeLa cervical cancer cells and HaCaT keratinocytes treated with H2, and a HeLa xenograft mouse model subjected to H2 inhalation were established. TUNEL, Cell Counting Kit­8 and Ki67 staining assays were used to detect cell apoptosis and proliferation. Oxidative stress was determined according to the levels of reactive oxygen species, malondialdehyde and superoxide dismutase. Tumor growth was recorded every 3 days, and the excised tumors were stained with hematoxylin and eosin. High­throughput RNA sequencing and subsequent Gene Ontology (GO) enrichment analysis were performed in HeLa­treated and un­treated HeLa cells. The expression of hypoxia­inducible factor (HIF)­1α and NF­κB p65 was verified by western blotting, immunohistochemistry and reverse transcription­quantitative PCR. The results revealed an increased apoptosis rate, and reduced cell proliferation and oxidative stress in H2­treated HeLa cells but not in HaCaT cells. Similarly, decreased tumor growth and cell proliferation, and enhanced cell apoptosis were observed in H2­treated HeLa tumors. RNA sequencing and GO analysis suggest that downregulated HIF1A (HIF­1α mRNA) and RelA (NF­κB p65) levels, and reduced NF­κB signaling were associated with the antitumor effect of H2. Finally, decreased HIF­1α and NF­κB p65 expression both at the transcriptional and translational levels were observed in H2­treated HeLa cells and in HeLa­derived tumors. In conclusion, the present study reveals a novel mechanism of H2 against cervical cancer, which may serve as a potential therapeutic target in clinical practice.

A Comparative Analysis of Robotic Single-Site Surgery and Laparoendoscopic Single-Site Surgery as Therapeutic Options for Stage IB1 Cervical Squamous Carcinoma.

PURPOSE: To compare perioperative outcomes between robotic single-site surgical technique and conventional laparoendoscopic single-site surgical technique. METHODS: This was a retrospective cohort study involving 67 patients who received robotic single-site surgery or laparoendoscopic single-site surgery for the treatment of stage IB1 cervical squamous carcinoma. The robotic single-site radical hysterectomy technique combined with pelvic lymph node dissections were performed in 32 patients while the laparoendoscopic single-site radical hysterectomy technique combined with pelvic lymph node dissections were performed in 35 patients. RESULTS: The enrolled patients had been diagnosed with stage IB1 cervical squamous carcinoma. The perioperative outcomes were mean age (51.63±8.32 years in the lymph node dissection (RSS group) and 53.14±8.14 years in the lymph node dissection (LESS group), p=0.453); BMIs (23.76±2.72 in the RSS group and 23.46±2.28 in the LESS group, p=0.629); shorter operative times (223.56±15.43 min in the RSS group and 248.61±20.89 min in the LESS group, p<0.01) and less estimated blood loss (217.25±16.77 mL in the RSS group and 294.74±24.00 mL in the LESS group, p<0.01). None of the study participants exhibited postoperative pain. There were no statistically significant differences in the length of hospital stay (p=0.865), perioperative complications (p=0.602), duration of closure and removal of catheter (p=0.518) as well as in pathological diagnoses between the two groups. CONCLUSION: Robotic single-site surgery can be used in the treatment of early stage cervical cancer as it exhibits acceptable operative times and perioperative outcomes. This surgical technique is feasible and safe.

Angiotensin (1-7) Attenuates Sepsis-Induced Acute Kidney Injury by Regulating the NF-κB Pathway.

This study explores the protective mechanism of angiotensin (1-7) [Ang-(1-7)] on kidneys by examining its effects on renal histomorphology, inflammatory response, oxidative stress, and NF-κB signaling in mice suffering from sepsis-induced acute kidney injury. A sepsis-induced acute kidney injury mouse model was established by intracervically injecting lipopolysaccharides (LPS group), followed by the administration of Ang-(1-7) [LPS + Ang-(1-7) group]. The serum levels of urea nitrogen, creatinine and cystatin. c were measured with an automatic biochemical analyzer, and changes in proinflammatory cytokines and angiotensin II (Ang II) in the serum and kidneys were quantified by enzyme-linked immunosorbent assays. Changes in oxidative stress indices in the renal cortex were detected by colorimetry. The localization of Ang II in kidneys was examined by immunohistochemistry. Western blotting was used to examine phosphorylated NF-κB-p65 and IκBα levels in kidneys. Compared with the control group, the serum levels of urea nitrogen, creatinine and cystatin. c were increased, whereas the levels of Ang II, TNFα, IL-1ß, IL-6, and malondialdehyde (mda) were increased significantly. The levels of Ang II and phosphorylated NF-κB-p65 were elevated in kidneys, whereas the levels of superoxide dismutase (sod), Total antioxidative capacity (TAOC), and inhibitor of NF-κB (IκBα) were reduced in the LPS group (p < 0.05). Pathological damage was also observed in kidneys of LPS-group mice. In Pearson correlation analysis, there was a positive correlation between Ang II and phosphorylated NF-κB-p65 levels, and a negative correlation between Ang II and IκBα levels (p < 0.05). After the application of Ang-(1-7), the levels of urea nitrogen, creatinine, cystatin. c, Ang II, TNFα, IL-1ß, IL-6, and mda, as well as the expression of Ang II and phosphorylated NF-κB-p65 in kidneys of LPS + Ang-(1-7)-group mice, were lower than those in kidneys of LPS-group mice, but the levels of sod, TAOC, and IκBα were higher than those of LPS-group mice (p < 0.05). Pathological changes were less severe in mice of the LPS + Ang-(1-7) group. Overall, Ang-(1-7) can decrease the Ang II level, inhibit NF-κB signaling, reduce the inflammatory response, decrease oxidative stress, and mitigate sepsis-associated acute kidney injury.