OBJECTIVE To study the protective effect and potential mechanism of chikusetsu saponin Ⅳ a （chsⅣ） on renal function in diabetic nephropathy （DN） model rats. METHODS DN rat model was established by high-fat diet combined with streptozotocin injection. Thirty-six model rats were randomly divided into model group （i.g. administration of normal saline， high-fat diet）， chsⅣ low-dose and high-dose groups （i.g. administration of 90， 180 mg/kg chsⅣ， high-fat diet）， with 12 rats in each group. Additionally， 10 normal rats were set as the control group （i.g. administration of normal saline， regular diet）. From the 5th to the 12th week after streptozotocin injection， they were given intragastric administration of relevant drug or normal saline， once a day. After the last medication， the levels of fasting blood glucose， fasting insulin， blood urea nitrogen， serum creatinine and urine protein as well as the levels of reduced glutathione （GSH）， superoxide dismutase （SOD） and malondialdehyde （MDA） in renal tissues were measured. Additionally， the insulin resistance index was calculated. Hematoxylin-eosin， periodic acid-Schiff， and Masson staining techniques were employed to examine the histopathological alterations in the renal tissue. The expressions of Notch signaling pathway-related proteins in renal tissue were detected by immunohistochemical staining and Western blot methods. RESULTS Compared with model group， the histomorphological of renal tissues in the chsⅣ low- and high-dose groups were significantly improved， with significant decreases in renal histological scores， mesangial expansion index， and glomerulosclerosis scores （ P ＜0.05）； the levels of fasting blood glucose， fasting insulin， blood urea nitrogen， serum creatinine， urine protein and homeostasis model assessment for insulin resistance， as well as MDA content， the expression levels of Notch1， Notch intracellular domain， hairy and enhancer of Split 1 and Delta-like protein 1 in renal tissue were all significantly decreased （ P ＜0.05）. The levels of GSH and SOD in renal tissue were significantly elevated （ P ＜0.05）. Moreover， the improvement in these indicators was significantly more pronounced in the chsⅣ high-dose group compared to the chsⅣ low-dose group （ P ＜0.05）. CONCLUSIONS ChsⅣ can ameliorate renal pathological damage and functional impairment in DN rats. Its underlying mechanisms include restoration of glucose homeostasis and insulin sensitivity， attenuation of renal oxidative stress， and suppression of aberrant Notch signaling pathway activation.

ObjectiveTo investigate the effect of interfering with long noncoding RNA （LncRNA） small nucleolar RNA host gene16 （SNHG16） on improving angiogenesis of ectopic endometrial stromal cells （EScs） in adenomyosis （AM） by targeting upregulation of miRNA （miR）-141-3p and inhibition of high mobility group box-1 protein （HMGB1）. MethodsThe expression levels of SNHG16， miR-141-3p and HMGB1 mRNA in endometrial tissues of 52 patients with adenomyosis （AM group） and 52 patients who needed hysterectomy due to cervical cancer or ovarian cancer （control group） were detected by quantitative reverse transcription polymerase chain reaction （qRT-PCR）. Y14 cells were divided into small hairpin RNA （shRNA） NC group， shRNA SNHG16 group， shRNA SNHG16+miR-141-3p inhibitor （inhibitor） group， shRNA SNHG16+inhibitor NC group and blank group. The targeting relationship between miR-141-3p and SNHG16 as well as HMGB1 was verified. The expression levels of SNHG16， miR-141-3p and HMGB1 mRNA in Y14 cells were detected by qRT-PCR. CCK-8 and Transwell assay were used to detect cell proliferation， invasion and migration. Microvascular density （MVD） was determined by immunofluorescence. The expressions of hypoxia-inducing factor α （HIF-1α）， cyclooxygenase-2 （Cox-2）， vascular endothelial growth factor （VEGF） and HMGB1 were detected by Western blot. ResultsThe expression of SNHG16 and HMGB1 mRNA in AM group was higher than that in control group， but the expression of miR-141-3p was lower than that in control group （P0.05）. The expression of SNHG16， HMGB1 mRNA， proliferation rate， migration， invasion number， MVD， expression of VEGF， HIF-1 α， Cox-2， and HMGB1 proteins in the shRNA SNHG16 group were lower than those in the blank group and shRNA NC group， while the expression of miR-141-3p was higher than that in the blank group and shRNA NC group （P0.05）. Inhibition of miR-141-3p reversed the improvement of EScs angiogenesis by interfering with SNHG16. ConclusionInterference with LncRNA SNHG16 improves EScs angiogenesis and inhibits proliferation， migration， and invasion of EScs by targeting upregulation of miR-141-3p and inhibition of HMGB1.

ObjectiveTo evaluate pharmacological effects of Shengmai injection（SMI）on cerebral ischemia and study its neuroprotective mechanism. MethodsMale specific pathogen-free （SPF） Sprague-Dawley （SD） rats were randomly divided into a sham group， a model group， a low-dose SMI group（3 mL·kg^-1）， a middle-dose SMI group（6 mL·kg^-1）， a high-dose SMI group（12 mL·kg^-1）， and a Ginaton group（4 mL·kg^-1）according to the random number table method， with 12 rats in each group. The rat model of cerebral ischemia-reperfusion（MCAO/R）was prepared via the suture method. The administration groups were intraperitoneally injected with corresponding concentrations of SMI or Ginaton injection after reperfusion， which was conducted for 3 consecutive days. The sham group and model group were administered the equivalent volume of physiological saline. The pharmacological effects of SMI on brain injury in MCAO/R rats were evaluated by neurological function scores， cerebral infarction area， hematoxylin-eosin （HE） staining， Nissl staining， terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） staining， and Western blot. The dominant link and key protein of SMI treating cerebral injury were explored using proteomic analysis. The related mechanisms of SMI were further validated using enzyme-linked immunosorbent assay （ELISA）， Western blot， and chloride ion fluorescence probe with oxygen-glucose deprivation/reoxygenation（OGD/R）-treated PC12 cells and MCAO/R rats. ResultsCompared with the sham group， the model group showed significantly increased neurological function scores， cerebral infarction area， neuronal apoptosis rate， and expression levels of apoptosis related proteins （P<0.05， P<0.01）and significantly decreased density of Nissl bodies and neurons（P<0.01）. Compared with the model group， the SMI groups exhibited significantly decreased neurological function scores， cerebral infarction area， neuronal apoptosis rate， and expression levels of apoptosis related proteins （P<0.05， P<0.01）and significantly increased density of Nissl bodies and neurons （P<0.05）. The proteomic analysis results showed that oxidative stress and inflammatory response were important processes of SMI intervening in MCAO/R injury， and the chloride intracellular channel protein 1 （CLIC1） was one of key proteins in its action network. The levels of representative indicators of oxidative stress and inflammatory response in the MCAO/R rats of the SMI groups were significantly reduced， compared with those in the model group（P<0.05， P<0.01）， and the expression levels of CLIC1 and downstream NOD-like receptor protein 3 （NLRP3） decreased （P<0.01）. In addition， the experimental results based on the OGD/R PC12 cells showed that SMI significantly increased the cell survival rate（P<0.01） and significantly decreased the intracellular chloride ion concentration（P<0.05）. ConclusionSMI has neuroprotective effects. Oxidative stress and inflammatory response are key processes of SMI intervening in MCAO/R injury. The potential mechanism is closely related to the regulation of CLIC1.

NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome mediates inflammation, induces pyroptosis, and regulates periodontal tissue remodeling through the maturation and secretion of its downstream cysteine protease 1 (Caspase-1)-dependent pro-inflammatory cytokines, interleukin (IL)-1β and IL-18. Orthodontic force mediates the aseptic inflammation of periodontal tissues and triggers adaptive alteration of periodontal tissues, thereby promoting the movement and stability of orthodontic teeth. NLRP3 inflammasome plays an important role in orthodontic tooth movement and causes periodontal tissue inflammation and orthodontic inflammatory root resorption in orthodontic patients. Literature review suggests that NLRP3 inflammasome is involved in the activation and differentiation of periodontal ligament fibroblasts, periodontal ligament stem cells, macrophages, osteoblasts, and osteoclasts in orthodontic tooth mobile tissue remodeling. Additionally, it targets the upstream nuclear factor kappa-B signaling pathway; downstream effectors, such as Caspase-1, IL-1β, and IL-18; and the NLRP3 inflammasome components for regulating tooth movement as well as treating and preventing orthodontics-associated periodontitis and orthodontic-induced inflammatory root resorption. Future studies can be focused on the specific mechanism of NLRP3 inflammasome tissue modification during orthodontic tooth movement. This article reviews the effects and regulatory mechanisms of the NLRP3 inflammasome signaling pathway on the corresponding tissue remodeling during orthodontic tooth movement.

Pulmonary endometriosis (PEM) is a rare disease with diverse clinical manifestations, most commonly presenting as hemoptysis, while patients presenting solely with pulmonary nodules are less common. Here, we report three female patients (aged 32, 19, and 46 years, respectively). One patient sought medical attention due to hemoptysis during menstruation, while the other two had no obvious symptoms and were found to have pulmonary nodules during routine physical examinations. Two patients had a history of cesarean section, and one had a history of miscarriage. Pathologically, one patient of PEM showed extensive hemorrhage in the alveolar spaces, with fragmented endometrial glandular epithelium observed within the hemorrhagic foci. The other two patients exhibited proliferative endometrial glands and stroma, surrounded by old hemorrhage. Immunohistochemistry revealed that the endometrial glands and stroma in all three patients were positive for estrogen receptor, progesterone receptor, and vimentin, with CD10 positivity in the endometrial stroma. All three patients were definitively diagnosed as PEM by pathology and underwent thoracoscopic pulmonary wedge resection. Follow-up periods were 18, 31, and 49 months, respectively, with no recurrence observed in any of the patients.

Objective To investigate the effect and mechanism of dabrafenib （DAB） combined with tremelimumab （TREM） on melanoma. Methods The effects of DAB combined with TREM on cell viability, cytotoxicity and cell migration of A375 cells were evaluated by Cell Counting Kit-8 （CCK-8） method, lactate dehydrogenase （LDH） method and scratch assay. The levels of reactive oxygen species （ROS）, adenosine triphosphate （ATP）, malondialdehyde （MDA）, and superoxide dismutase （SOD） were detected to evaluate the effects of combined drugs on oxidative stress and energy metabolism. In addition, A375 tumor-bearing nude mice model was used to evaluate the inhibitory effect of the combined treatment on tumor growth in vivo, and the degree of cell apoptosis and cell proliferation in tumor tissues were analyzed by terminal deoxynucleotidyl transferase-mediated dutP Nick end labeling （TUNEL） and proliferating cell nuclear antigen （PCNA） immunohistochemical staining. Results The combined treatment significantly inhibited the survival rate and migration ability of A375 cells and enhanced the cytotoxicity. The combined intervention also significantly increased ROS level, decreased ATP, SOD and MDA levels. It effectively inhibited tumor growth in tumor-bearing nude mice, increased the apoptosis rate of tumor cells and inhibited cell proliferation. Conclusion DAB combined with TREM may improve the therapeutic effect of melanoma by enhancing oxidative stress, inhibiting energy metabolism, and promoting cell apoptosis. This combination therapy may provide a new therapeutic strategy to overcome the limitations of singledrug therapy.

ObjectiveTo investigate the protective effects and mechanisms of Bushen Zhuyun prescription （BSZY） on abortion rats with kidney deficiency-corpus luteum inhibition syndrome. MethodsAn abortion rat model with kidney deficiency-corpus luteum inhibition syndrome was constructed. Pregnant mice aged 8-10 weeks were randomly divided into a control group （Control）， a model group （Model）， low-dose BSZY （BSZY-L）， medium-dose BSZY （BSZY-M）， and high-dose BSZY （BSZY-H） groups （2.57， 5.14， 10.28 g·kg^-¹）， and a Zishen Yutai Pill （ZSYT） group （1.575 g·kg^-¹）. Hematoxylin-eosin （HE） staining was used to evaluate histopathological changes in ovarian and decidual tissue of rats in each group. Enzyme-linked immunosorbent assay （ELISA） was employed to measure levels of estrogen （E₂）， progesterone （P）， luteinizing hormone （LH）， prolactin （PRL）， and follicle-stimulating hormone （FSH） in serum. The candidate targets of BSZY were obtained from the Traditional Chinese Medicine System Pharmacology Platform （TCMSP） and Integrative Pharmacology-based Research Platform of Traditional Chinese Medicine （TCMIP） v2.0 databases， while disease targets for recurrent spontaneous abortion （RSA） were retrieved from GeneCards， DrugBank， Online Mendelian Inheritance in Man （OMIM）， and Therapeutic Target Database （TTD）. The intersection targets were identified by the Venny 2.1.0 platform. Pathway enrichment analysis was conducted based on the Metascape database to predict the potential mechanisms of BSZY. Additionally. Western blot was used to verify the effects of BSZY on the expression of estrogen receptor （ERα）， phosphatidylinositol 3-kinase （PI3K）， and protein kinase B （Akt） and explore its protective mechanism on RSA rats. ResultsCompared with the control group， the model group exhibited significantly decreased uterine， ovarian， and embryonic wet weights （P<0.05， P<0.01）， with an abortion rate of 57.18%. The ovarian tissue showed varying degrees of reduction in primordial follicles， primary follicles， mature follicles， and corpora lutea， along with a large number of atretic follicles. The endometrium was thinner， and decidual tissue exhibited cellular edema and disorganized arrangement. In contrast， compared with the model group， the BSZY groups at all doses and the ZSYT group demonstrated increased uterine， ovarian， and embryonic wet weights， along with a reduced abortion rate. The number of primordial follicles， primary follicles， mature follicles， and corpora lutea increased， while atretic follicles decreased. The endometrium thickened， and decidual tissue displayed normal cellular structure with tight arrangement. Additionally， the model group showed significantly decreased levels of E₂， P， PRL， and FSH in serum （P<0.05， P<0.01）， along with a decreasing trend in LH level. In contrast， the BSZY groups at all doses exhibited significantly elevated levels of E₂， P， LH， PRL， and FSH in serum （P<0.05， P<0.01）. Network pharmacology predictions suggested that BSZY may exert protective effects against abortion in rats by activating the ERα/PI3K/Akt signaling pathway. Western blot results confirmed that BSZY significantly upregulated the expression of ERα， PI3K， and p-Akt proteins （P<0.05， P<0.01）. ConclusionBSZY has a protective effect on the abortion rats with kidney deficiency-corpus luteum inhibition syndrome， possibly by activating the ERα/PI3K/Akt signaling pathway to reduce ovarian apoptosis and regulate endocrine function， thereby lowering the abortion rate.

The paper reports acupuncture treatment for one case of oculomotor nerve palsy after cranial-orbital communicating tumor surgery. The acupoint prescription was composed of the local acupoints of the eyes (Yansanzhen, Tijian, Cuanzhu [BL2], Yuyao [EX-HN4] and Sizhukong [TE23]), the acupoints on the head, face and neck (Yangbai [GB14], Sibai [ST2] and Fengchi [GB20]), Guanyuan (CV4) on the abdomen, and those on the four limbs (Hegu [LI4], Zusanli [ST36], Shenmai [BL62] and Zhaohai [KI6]). The point-to-point needling technique with the eyelid lifted was operated at Tijian, Cuanzhu (BL2), Yuyao (EX-HN4), and Sizhukong (TE23). Warm needling with moxa cone placed on the needle handle was operated at Guanyuan (CV4) and Zusanli (ST36), and the usual needling technique was delivered at the rest acupoints. The treatment was given once daily, discontinued for 1 day after every 6 treatments. One course of treatment was composed of 7 days, and 6 courses were required. After treatment completion, the upper eyelids were basically symmetrical and the bilateral eye cracks were equal, the double vision appeared occasionally. No recurrence and no aggravation were reported in 1 month of follow up visit.
Humans ; Acupuncture Points ; Acupuncture Therapy ; Oculomotor Nerve Diseases/etiology* ; Orbital Neoplasms/surgery* ; Postoperative Complications/etiology*

Heritable aortic disease (HAD) is characterized by thoracic aortic aneurysm/dissection with strong genetic predisposition and high clinical phenotypic heterogeneity. HAD is one of the main causes of sudden death. Early diagnosis of this disease is difficult because of atypical clinical symptoms, leading to the deterioration of disease with the development of aortic aneurysm, aortic dissection or sudden death. Genetic testing plays an important role in the early diagnosis, standardized follow-up, screening of family members, genetic counseling and individualized treatment of HAD. This review focused on the application of genetic testing in the standardized diagnosis and treatment of HAD.

Objective To assess the clinical value of a novel surgical technique—Tubeless subxiphoid uniportal video-assisted thoracoscopic surgery with percutaneous suspension technique via balance-shaped sternal elevation device in the resection of anterior mediastinal masses. Methods Patients who underwent tubeless subxiphoid uniportal video-assisted thoracoscopic surgery via balance-shaped sternal elevation device in anterior mediastinal masses process at the Department of Thoracic Surgery, West China Hospital, Sichuan University from March to April 2025 were included, and their clinical data were analyzed. Results A total of 4 patients were included, with 2 males and 2 females, aged 58-75 years. The diameter of the tumor was 2.5-3.0 cm. The operation time was 60.0-150.0 min, intraoperative blood loss was 5-10 mL, pain score on the 3rd day after surgery was 0 points, and postoperative hospital stay was 2-3 days. All patients achieved complete resection of the masses and thymus without perioperative complications. Conclusion The tubeless subxiphoid uniportal video-assisted thoracoscopic surgery with percutaneous suspension technique via balance-shaped sternal elevation device technique optimizes surgical visualization and instrument maneuverability while avoiding complications related to conventional anesthesia and tubing, thereby markedly enhancing the minimally invasive profile of anterior mediastinal masses resections. In addition to maintaining procedural safety, this approach effectively reduces postoperative pain and accelerates patient recovery, highlighting its potential for widespread clinical adoption.