Inadequate vascularization represents a major obstacle to wound healing by limiting the delivery of essential nutrients and oxygen. To overcome this limitation, crocetin (Cro), an active component of traditional Chinese medicine, is loaded onto calcium peroxide (CaO2)-based nanoparticles via electrostatic interactions to construct a nanodelivery system (CP@Cro nanoparticles) for evaluating its angiogenic potential. The CP@Cro nanoparticles exhibit pH-responsive degradation and sustained release of calcium ions, oxygen, and crocetin. They demonstrate excellent biocompatibility with Human Umbilical Vein Endothelial Cells (HUVECs) while preserving the bioactivity of crocetin, which promoted cell proliferation and migration in a controlled manner. Notably, extensive tube formation is observed in HUVECs after only 4 h of culturing with CP@Cro nanoparticles in vitro, attributed to the upregulation of vascular endothelial growth factor (VEGF) and zonula occludens-1 (ZO-1) proteins. Meanwhile, freely released calcium ions and oxygen appear to act synergistically to enhance tube formation. Furthermore, crocetin promotes the differentiation of HUVECs into tip endothelial cells, a process that is synergistically amplified by the controlled delivery afforded by CP@Cro nanoparticles. These findings highlight the promising pro-angiogenic functions of crocetin and CP@Cro nanoparticles and indicate a potential therapeutic strategy combining traditional Chinese medicine with nanodelivery systems to promote vascular regeneration.

METTL3, a key RNA N6-methyladenosine (m6A) methyltransferase, plays essential roles in cell fate regulation and tissue homeostasis, yet therapeutic strategies to enhance its activity remain unexplored. Here, we profile the S-palmitoylation landscape during embryonic stem cell differentiation and observe increased METTL3 S-palmitoylation at cysteine 376 during mesodermal commitment. This modification is catalyzed by ZDHHC24 and reversed by ABHD17A. METTL3 C376S mice exhibit cartilage defects and exacerbated osteoarthritis (OA). Through AI-guided screening, we identify Isoborneol as a small molecule that enhances METTL3 S-palmitoylation by disrupting its interaction with ABHD17A. Isoborneol treatment alleviates joint degeneration and preserves cartilage integrity in OA models. Mechanistically, S-palmitoylation promotes METTL3 condensate formation in proximity to ribosomes, facilitating its cytoplasmic spatial compartmentalization. This condensate state suppresses chaperone-mediated autophagy, thereby enhancing METTL3 protein stability. Our findings reveal S-palmitoylation as a regulatory mechanism governing METTL3 localization and turnover and establish a pharmacological strategy for restoring METTL3 activity in OA.

Mesenchymal stem cells (MSCs) are multipotent stem cells that have a chondrogenic differentiation capacity. However, the molecular mechanism underlying the chondrogenic differentiation of MSCs has not been fully elucidated, which hinders further development of MSC-based cell therapies for cartilage repair in the clinic. Here, we showed that the E3 ubiquitin ligase Trim63 positively regulates the chondrogenic differentiation of MSCs by catalyzing the K27-linked cysteine ubiquitination of Myh11. Trim63 directly interacts with Myh11 and catalyzes K27-linked ubiquitination of cys382. Mutation of cys382 diminishes Trim63-catalyzed K27-linked ubiquitination and chondrogenic differentiation of MSCs. A deficiency in Trim63 significantly impairs the chondrogenic differentiation of MSCs. Trim63 enhances the repair of articular cartilage defects in vivo. Taken together, the results of our study demonstrated that Trim63 promotes the chondrogenic differentiation of MSCs by catalyzing K27-linked cysteine ubiquitination of Myh11, which provides an alternative therapeutic target for cartilage regeneration and repair.

Diabetic wound (DW) complications, driven by persistent oxidative stress, unresolved inflammation, and vascular dysfunction, present a critical clinical challenge. Given mitochondria's pivotal role in inflammatory regulation, intercellular mitochondrial transfer emerges as a promising therapeutic target for DW management. In this study, we engineered a ROS/glucose/pH-triple responsive nanoplatform (WOC) via coordination-driven assembly of tungstate anions (WO4 2-) and chitosan oligosaccharide (COS) to synchronize immunomodulation and angiogenesis for adaptive DW regeneration. The WOC platform demonstrated glucose/pH-triggered release of bioactive components with moderate ROS scavenging capacity, enabling real-time monitoring via visible colorimetric transition. By enhancing mitochondrial bioenergetics, WOC polarized macrophages to M2 phenotype and orchestrated vesicles-dependent mitochondrial transfer to injured endothelial cells, restoring vascular function through upregulated angiogenesis genes, enhanced migration, and tube formation. In diabetic rat models, WOC accelerated wound closure evidently, resolving inflammation and promoting scarless regeneration via balanced collagen deposition. This work establishes mitochondrial transfer as a promising strategy, offering a tunable nanotherapeutic approach to recalibrate cellular cross-talk and microenvironment dynamics in DW healing.

Hair follicle stem cells (HFSCs) can quickly activate and migrate to the wound site, differentiating into epidermal stem cells to facilitate early epithelialization. During the wound healing process, microRNAs (miRNAs) function coordinately. Chinese medicine borneol is derived from the Cinnamomum camphora plant, and its principal component, L-borneol, is renowned for its potential in facilitating skin wound healing. However, it remains unclear whether L-borneol can stimulate HFSCs to differentiate into epidermal cells or whether miRNAs are involved in this process. In the current study, HFSCs were isolated from the vibrissae of rats and identified based on the expression of CD34, Integrin-β1 and keratin type 1 cytoskeletal 15(CK15). We observed that stimulation with L-borneol significantly increased the differentiation marker K14 in HFSCs, suggesting that L-borneol could promote the differentiation of HFSCs into basal layer cells. On this basis, we transfected and confirmed that rno-miR-127 inhibitor could promote the differentiation of HFSCs. Furthermore, we demonstrated that PODXL2 is a target gene of rno-miR-127 through dual-luciferase reporter assays and confirmed that the rno-miR-127 mimic could inhibit the expression of PODXL2. To further elucidate the targeting relationship, we constructed the siPODXL2 fragment using siRNA technology, demonstrating that reducing PODXL2 expression can inhibit the differentiation of HFSCs into basal layer cells. Finally, a rat full-thickness skin defect model illustrated L-borneol-mediated negative regulation of PODXL2 by rno-miR-127, promoting skin injury repair through HFSCs.

Geraniin, a chemical component of the traditional Chinese medicine geranii herba, possesses anti-inflammatory and anti-oxidative activities. However, its anti-inflammatory role in managing NLRP3 inflammasome and pyroptosis remains to be elucidated. To investigate the anti-inflammation mechanism of geraniin, LPS-primed macrophages were incubated with classical activators of NLRP3 inflammasome (such as ATP, Nigericin, or MSU crystals), and MSU crystals were injected into the ankle joints of mice to establish an acute gouty arthritis model. The propidium iodide (PI) staining results showed that geraniin could restrain cell death in the ATP- or nigericin-stimulated bone marrow-derived macrophages (BMDMs). Geraniin decreased the release of lactate dehydrogenase (LDH) and interleukin (IL)-1β from cytoplasm to cell supernatant. Geraniin also inhibited the expression of caspase-1 p20, IL-1β in cell supernatant and N-terminal of gasdermin D (GSDMD-NT) while blocking the oligomerization of ASC to form speck. The inhibitory effects of geraniin on caspase-1 p20, IL-1β, GSDMD-NT, and ASC speck were not observed in NLRP3 knockout (NLRP3-/-) BMDMs. Hence, the resistance of geraniin to inflammasome and pyroptosis was contingent upon NLRP3 presence. Geraniin reduced reactive oxygen species (ROS) production and maintained mitochondrial membrane potential while preventing interaction between ASC and NLRP3 protein. Additionally, geraniin diminished MSU crystal-induced mouse ankle joint swelling and IL-1β expression. Geraniin blocked the recruitment of neutrophils and macrophages to the synovium of joints. Our results demonstrate that geraniin prevents the assembly of ASC and NLRP3 through its antioxidant effect, thereby inhibiting inflammasome activation, pyroptosis, and IL-1β release to provide potential insights for gouty arthritis targeted therapy.

Atherosclerosis is a chronic inflammatory disease characterized by endothelial dysfunction and plaque formation. Under pro-inflammatory conditions, endothelial cells can undergo endothelial-to-mesenchymal transition (EndMT), contributing to atherosclerosis development. However, the specific regulatory mechanisms by which EndMT contributes to atherosclerosis remain unclear and require further investigation. Dan-Shen-Yin (DSY), a traditional Chinese herbal formula, is commonly used for cardiovascular diseases, but its molecular mechanisms remain elusive. Emerging evidence indicates that competing endogenous RNA (ceRNA) networks play critical roles in atherosclerosis pathogenesis. In this study, we constructed an EndMT-associated ceRNA network during atherosclerosis progression by integrating gene expression profiles from the Gene Expression Omnibus (GEO) database and weighted gene co-expression network analysis. Functional enrichment analysis revealed this EndMT-related ceRNA network is predominantly involved in inflammatory responses. ROC curve analysis showed the identified hub genes can effectively distinguish between normal vasculature and atherosclerotic lesions. Furthermore, Kaplan-Meier analysis demonstrated that high expression of IL1B significantly predicts ischemic events in atherosclerosis. Molecular docking revealed most DSY bioactive components can bind key EndMT-related lncRNAs, including AC003092.1, MIR181A1HG, MIR155HG, WEE2-AS1, and MIR137HG, suggesting DSY may mitigate EndMT in atherosclerosis by modulating the ceRNA network.

Our recent study demonstrated that knockout of microRNA-301a attenuates migration and phagocytosis in macrophages. Considering that macrophages and Schwann cells synergistically clear the debris of degraded axons and myelin during Wallerian degeneration, which is a prerequisite for nerve regeneration, we hypothesized that microRNA-301a regulates Wallerian degeneration and nerve regeneration via impacts on Schwann cell migration and phagocytosis. Herein, we found low expression of microRNA-301a in intact sciatic nerves, with no impact of the microRNA-301a knockout on nerve structure and function. By contrast, we found significant upregulation of microRNA-301a in injured sciatic nerves. We established a sciatic nerve crush model in microRNA-301a knockout mice, which exhibited attenua9ted morphological and functional regeneration following sciatic nerve crush injury. The microRNA-301a knockout also led to significantly inhibited Wallerian degeneration in an in vivo sciatic nerve-transection model and in an in vitro nerve explant block model. Schwann cells with the microRNA-301a knockout showed inhibition of phagocytosis and migration, which was reversible under transfection with microRNA-301a mimics. Rescue experiments involving transfection of microRNA-301a-knockout Schwann cells with microRNA-301a mimics or treatment with the C-X-C motif receptor 4 inhibitor WZ811 indicated the mechanistic involvement of the Yin Yang 1/C-X-C motif receptor 4 pathway in the role of microRNA-301a. Combined with our previous findings in macrophages, we conclude that microRNA-301a plays a key role in peripheral nerve injury and repair by regulating the migratory and phagocytic capabilities of Schwann cells and macrophages via the Yin Yang 1/C-X-C motif receptor 4 pathway.

Vascular dementia (VD) was characterized by both motor and non-motor dysfunctions and accounts for approximately 20% of dementia patients. Although VD has been given enormous attention owing to its high morbidity and severe consequence, the pathologic mechanisms of VD remain unclear. In this study, the bilateral common carotid artery occlusion (2-VO) rat, which has similar symptoms to VD,was explored the effect of miRNAs and the correlation between ferroptosis and Egl nine homolog 2 (EGLN2) in VD. RT-qPCR showed that miR-161, a new miRNA found in the 2-VO rat, was down-regulated in the frontal lobe, concomitant with increased EGLN2 expression.Western blotting and immunohistochemistry staining results showed, compared with control, the expression of EGLN2 has a significant increase consistently. Target prediction analysis and luciferase-3'‑untranslated region (3’UTR) reporter assay identified the 3’UTR of EGLN2 mRNA to be the direct target of miR-161. Compared with miR-161 treatment, miR-161 inhibition resulted in higher EGLN2 expression. To further explore the role of EGLN2, bioinformatics was used to screen genes. The results showed that glutathione-dependent antioxidant enzyme glutathione peroxidase 4 (GPX4) expression is significantly lower in the brains of VD patients than those in the normal brain. The results of protein interaction analysis showed that GPX4 and EGLN2 could interact with each other. Further experimental results showed, the expression of GPX4 was downgrade in vivo. For PC12 cells, the effect of EGLN2 silencing was consistent with miR-161 decreased GPX4 levels. In conclusion, multiple experimental results elucidated that miR-161 regulates ferroptosis by targeting EGLN2 expression in the frontal lobe which provides a perspective to develop a potential new therapeutic strategy for VD.

The ideal and highly anticipated dressing for skin wounds should provide a moist environment, possess antibacterial properties, and ensure sustained drug release. In the present work, a hyaluronic acid-based hydrogel was formed by cross-linking crocetin and CaCO3@polyelectrolyte materials (CaCO3@PEM) microspheres with HA hydrogels via hydrogen bond and amido bonding (CaCO3@PEM@Cro@HA hydrogel, CPC@HA hydrogel). Moreover, the CPC@HA hydrogel had the capability of sustained, controlled release of calcium ions and crocetin via pH-sensitive and accelerated skin wound healing. The experiment results showed that the CPC@HA hydrogel exhibited porous network structures, stable physical properties, and had antibacterial properties and biocompatibility in vitro. In addition, the CPC@HA hydrogel covering on the skin wound could reduce inflammation and promote wound healing. The high expression of angiogenic cytokines (CD31) and epidermal terminal differentiation markers (Loricrin) of wound healing tissue suggested the CPC@HA hydrogel also had the function of promoting the remodeling of regenerated skin. Overall, CPC@HA hydrogel has promising potential for clinical applications in accelerating skin wound repair.

Atractylenolide-III (AT-III) is well known as its role in antioxidant and anti-inflammatory. Present study was aimed to figure out its effects on osteoarthritis and potential mechanisms. Rat model, human osteoarthritis cartilage explants as well as rat/human chondrocyte cultures were prepared to test AT-III's effects on osteoarthritis progression and chondrocyte senescence. Potential targeted molecules of AT-III were predicted using network pharmacology and molecular docking, assessed by Western blotting and then verified with rescue experiments. AT-III treatment alleviated osteoarthritis severity (shown by OARSI grading score and micro-CT) and chondrocyte senescence (indexed by levels of SA-β-gal, P16, P53, MMP13, ROS and ratio of healthy/collapsed mitochondrial membrane potentials). Network pharmacology and molecular docking suggested that AT-III might play role through NF-κB pathway. Further experiments revealed that AT-III reduced phosphorylation of IKKα/β, IκBα and P65 in NF-κB pathway. As well as nuclear translocation of p65. Both in vivo and in vitro experiments indicated that AT-III's effects on osteoarthritis and anti-senescence were reversed by an NF-κB agonist. AT-III could alleviate osteoarthritis by inhibiting chondrocyte senescence through NF-κB pathway, which indicated that AT-III is a prospective drug for osteoarthritis treatment.

Objective Functional polymorphisms of interleukin 16 (IL16) have been reported to be closely related to the risk of osteoarthritis (OA). However, how IL16 affects OA remains unclear. In this study, the role of IL16 in OA and the possible mechanisms were examined. Methods We established a meniscal/ligament injury (MLI) post-traumatic OA model in Sprague Dawley rats and an IL1β-induced ADTC5 cells OA model. We detected the expression of IL16, novel-miR-81, MMP3, and MMP13 by quantitative real-time polymerase chain reaction. Western blot was performed to detect the expression of IL16, MMP3, and MMP13. The association between IL16 and novel-miR-81 was confirmed by luciferase reporter assay. Hematoxylin and eosin staining, Safranin O and Fast Green staining, and immunohistochemical staining were performed to clarify the effect of intra-articular injection of novel-miR-81 agomir in rats OA model. Results IL16 was upregulated in OA model. Knockdown of IL16 and overexpression of novel-miR-81 downregulated the expression of MMP3 and MMP13. Importantly, IL16 was a key target of novel-miR-81. Intra-articular injection of novel-miR-81 agomir could attenuate OA progression in rats OA model. Conclusion Novel-miR-81 targeted IL16 to relieve OA, suggesting that novel-miR-81and IL16 may be new therapeutic targets for OA.

Background and Objectives: Osteoarthritis (OA) is a degenerative disease that leads to the progressive destruction of articular cartilage. Current clinical therapeutic strategies are moderately effective at relieving OA-associated pain but cannot induce chondrocyte differentiation or achieve cartilage regeneration. We investigated the ability of wedelolactone, a biologically active natural product that occurs in Eclipta alba (false daisy), to promote chondrogenic differentiation. Methods and Results: Real-time reverse transcription-polymerase chain reaction, immunohistochemical staining, and immunofluorescence staining assays were used to evaluate the effects of wedelolactone on the chondrogenic differentiation of mesenchymal stem cells (MSCs). RNA sequencing, microRNA (miRNA) sequencing, and isobaric tags for relative and absolute quantitation analyses were performed to explore the mechanism by which wedelolactone promotes the chondrogenic differentiation of MSCs. We found that wedelolactone facilitates the chondrogenic differentiation of human induced pluripotent stem cell-derived MSCs and rat bone-marrow MSCs. Moreover, the forkhead box O (FOXO) signaling pathway was upregulated by wedelolactone during chondrogenic differentiation, and a FOXO1 inhibitor attenuated the effect of wedelolactone on chondrocyte differentiation. We determined that wedelolactone reduces enhancer of zeste homolog 2 (EZH2)-mediated histone H3 lysine 27 trimethylation of the promoter region of FOXO1 to upregulate its transcription. Additionally, we found that wedelolactone represses miR-1271-5p expression, and that miR-1271-5p post-transcriptionally suppresses the expression of FOXO1 that is dependent on the binding of miR1271-5p to the FOXO1 3'-untranscribed region.Conclusions: These results indicate that wedelolactone suppresses the activity of EZH2 to facilitate the chondrogenic differentiation of MSCs by activating the FOXO1 signaling pathway. Wedelolactone may therefore improve cartilage regeneration in diseases characterized by inflammatory tissue destruction, such as OA.

ObjectiveMicroRNAs (miRNAs) play a key role in the differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) into chondrocytes. Our previous study found that novel-miR-81 can relieve osteoarthritis, but its role in chondrogenic differentiation of BMSCs remains unclear. The purpose of this study was to explore the role of novel-miR-81 in chondrogenic differentiation of BMSCs.MethodsWe used a model in which transforming growth factor (TGF)-β3-induced BMSCs differentiation into chondrocytes. We detected the expression Sox9, Collagen Ⅱ, Aggrecan, novel-miR-81, and Rac2 by real-time reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Western blot was performed to detect the expression of Sox9, Collagen Ⅱ, and Rac2. Dual-luciferase reporter gene assay confirmed that the association between novel-miR-81 and Rac2. In addition, the ectopic chondrocyte differentiation of BMSCs was performed subcutaneously in nude mice. The effect of novel-miR-81 and Rac2 on ectopic chondrogenic differentiation of BMSCs was determined by immunohistochemical staining.ResultsNovel-miR-81 upregulated in chondrogenic differentiation of BMSCs. Rac2 was a key target of novel-miR-81. Mimic novel-miR-81 and siRac2 upregulated the expression of Sox9, Collagen Ⅱ, and Aggrecan.ConclusionNovel-miR-81 promotes the chondrocytes differentiation of BMSCs by inhibiting the expression of target gene Rac2, which provides potential targets for BMSCs transplantation to repair cartilage defects.

Bone marrow mesenchymal stem cells (BMSCs) have the ability to differentiate into chondrocytes. In the differentiation of BMSCs into chondrocytes, micro-RNAs (miRNAs) play an important role. rno-miR-90 is a new miRNA discovered by our research team, and its role in chondrogenic differentiation of BMSCs is unknown. This study aimed to investigate whether rno-miR-90 could promote chondrogenic differentiation of BMSCs by regulating secreted protein acidic and rich in cysteine-related modular calcium binding 2 (Smoc2). First, BMSCs chondroblast differentiation was successfully induced in vitro by classical induction method of transforming growth factor (TGF)-β3. On this basis, we transfected rno-miR-90 mimic and inhibitor, and confirmed that rno-miR-90 mimic could promote the differentiation of BMSCs into chondrocytes by real-time reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting. In addition, we demonstrated that Smoc2 was a target gene of rno-miR-90 by dual-luciferase reporter assay, and confirmed that rno-miR-90 mimic could inhibit the expression of Smoc2 by RT-qPCR and western blotting. In order to further prove the targeting relationship between rno-miR-90 and Smoc2, we constructed three interfering fragments of Smoc2, and proved that silencing Smoc2 could promote the differentiation of BMSCs into chondrocytes at the transcriptional and protein levels. Finally, we constructed a carrier scaffold for ectopic chondrogenic differentiation in vivo, and confirmed that rno-miR-90 mimic and siSmoc2 could promote chondrogenic differentiation of BMSCs by Alcian blue staining and immunohistochemistry. In summary, our results suggested that rno-miR-90 could promote chondrogenic differentiation of BMSCs by down-regulating the expression of Smoc2. rno-miR-90 mimic and Smoc2 may be therapeutic targets of osteoarthritis.

Background:There is currently no effective treatment for vascular dementia (VaD). Scalp electroacupuncture (EA) has served clinically as an alternative treatment for VaD, but its mechanism is still unclear. In this study, we investigated the effect of EA at the Baihui (GV 20) and Shenting (GV 24) acupoints on spatial learning and memory ability, and the expression level of microRNA-81 (miR-81), interleukin-16 (IL-16), and postsynaptic density protein-95 (PSD-95) in the frontal cortex of VaD rats.Methods:Male Sprague-Dawley rats were randomly divided into four groups, sham, VaD, non-acupuncture (non-AP) and EA group. The VaD model was established by permanent bilateral occlusion of the common carotid arteries. Morris Water Maze was used to assess the rats' spatial learning and memory. Immunochemistry (IHC), quantitative reverse transcription polymerase chain reaction (qRT-PCR), and western blot analysis were performed to detect the expression level of miR-81, IL-16, and PSD-95. Finally, luciferase assay was used to determine the effect of miR-81 on IL-16 expression in PC12 cells.Results:The space exploration experiment of MWM showed the time and distance of the rat's activities around the platform were decreased in the EA group. Compared to the VaD and non-AP group, the number of terminal deoxynucleotidyl transferase-mediated dUDP nick-end labeling (TUNEL)-positive frontal cortical neurons was significantly decreased in EA group. The number of the PSD-95-positive cells and the miR-81 expression level in the frontal cortical in the EA group was dramatically increased in comparison with the other groups. In the PC12 cell validation experiment, IL-16 expression level was reduced under the condition of the miR-81 mimic treatment, while increased in the miR-81 inhibitor group. The PSD-95 protein level was up-regulated in the small interfering (si)RNA-IL16 group compared to the NC-IL16 groups with or without oxygen/glucose deprivation/reperfusion (OGD/R) conditions (P<0.05). However, this was abolished by miR-81 mimic.Conclusions:In VaD rats, EA may improve spatial learning and memory through miR-81/IL-16/PSD-95 pathway.

Abstract Background: Diabetic ulcers are a major complication of diabetes which causing lower extremity amputation. Nonetheless, the progression in the development of diabetic ulcers therapeutics is slow. Ferroptosis plays a key role in the pathogenesis of chronic wound in diabetic ulcers. The mechanism needs to be further clarified. Methods: Ferroptosis-related differentially expressed genes (FRDEGs) in diabetic ulcers were screened from the dataset GSE92724 and FerrDb online database based in silico. Then, functional enrichment analysis and protein-protein interaction (PPI) network were implemented to recognize the potential biological pathways and mechanisms. MCODE tool was used to cluster and predict hub genes. The miRNAs corresponding to hub genes were predicted by miRWalk 2.0. Receiver operating characteristic (ROC) was applied to verify the diagnostic value of five hub genes in the dataset GSE132187 and GSE134431. The immune infiltration between diabetic ulcers samples and normal samples were analyzed by using CIBERSORTx. Results: 26 FRDEGs and 5 hub genes (EGFR, SLC2A1, CD44, CA9, and PTGS2) in diabetic ulcers were identified. GO and KEGG analysis revealed that hub genes were significantly enriched in response to oxidative stress, basolateral plasma membrane, and HIF-1 signaling pathway. ROC results suggested that hub genes have a high diagnostic accuracy for diabetic ulcers. In immune cell infiltration, T follicular helper cells and monocytes were significantly lower in diabetic ulcers. Conclusion: This research firstly demonstrated that five hub genes may be potential therapeutic targets and possible diagnostic biomarkers in the pathogenesis of diabetic ulcers.

ObjectiveToanalyzethecorrelationbetweenserumbrainnatriureticpeptide（ BNP）levelandprognosisofelder lypatientswithpulmonaryembolism.Methodstheclinicaldataof70elderlypatientswithpulmonaryembolismtreatedinourhospita lwereretrospectivelyanalyzed.20patientswithoutadverseprognosticeventswereincludedinthegoodprognosisgroupand50patie ntswithadverseprognosticeventswereincludedinthebadprognosisgroup.ThedifferencesbetweenBNPlevelandgeneraldatabet weenthetwogroupswereobserved，andthecorrelationbetweenBNPandprognosiswasanalyzed.ResultsTherewasnodifferencebe tweenthehistoryofage，gender，hypertension，diabetes，hyperlipidemiaandsmoking，andtheproportionofpatientsintheg oodprognosiswassignificantlylowerthanthoseinthepoorprognosis，andtheaverageBNPlevelandtroponinlevelweresignificantl ylowerthanthoseinthepoorprognosis，andthecomparisonwasdifferent.Conclusionthecommonadverseprognosisofelderlypatie ntswithpulmonaryembolismincludesthrombolytictherapy，cardiogenicshockanddeath.Earlyprognosisevaluationcaneffectiv elypreventandcontroltheadverseprognosis.Thisstudyconfirmedthatbrainnatriureticpeptidelevelcanbeusedasakeyindexforpr ognosisevaluationofelderlypatientswithpulmonaryembolism.Inaddition，thereisalsoacertaincorrelationbetweentroponin， cardiacfunctionandprognosis.