Pathological Changes In Tissues Research Articles

Hydrocephalus in Connection to Genetic Mutation in Cranial Neural Crest Cells.

Hydrocephalus, a pathological condition due to the accumulation of cerebrospinal fluid (CSF) in the brain's ventricles, has been recognised as a relatively common brain abnormality in newborns and young adults with or without craniofacial anomaly. It can cause physical, behavioural and cognitive symptoms and, in severe cases, may result in lethality. Hydrocephalus can result from various underlying conditions, and its multifactorial nature makes pinpointing a single pathophysiological aetiology challenging. Notably, the relatively high prevalence of hydrocephalus (up to 100%) in the cranial neural crest cells (CNCCs) conditional knockout mouse models of various genes using Wnt1-Cre has been reported, given the extremely low (0.01% to 0.86%) spontaneous occurrence of hydrocephalus in different strains of lab mice. Surprisingly, there were no reports on the connections of hydrocephalus with CNCCs, although the prominent role of CNCCs in normal development and pathologic conditions of craniofacial and neural tissues has been extensively studied and highly recognised. In this review, besides revealing the high prevalence of hydrocephalus (5.4%-100%), we primarily summarised the invivo findings of hydrocephalus and the associated pathological changes of brain and craniofacial skeletal tissues with the genetically modified mouse (GMM) models of various genes knocked out in CNCCs. Significantly, the functional gene knockout in Wnt1 expressing cells can lead to hydrocephalus and associated brain and craniofacial skeletal pathologies, irrespective of the ectopic midbrain Wnt1 activation observed in Wnt1-Cre driver mice. However, the specific contributions and underpinning mechanisms of the main structures of the CSF system, including CNCCs-derived choroid plexus, to hydrocephalus pathophysiology are yet to be fully elucidated.

Multiplex imaging of amyloid-β plaques dynamics in living brains with quinoline-malononitrile-based probes.

The dynamic behaviour of amyloid-β (Aβ) plaques in Alzheimer's disease remains poorly understood, and accumulation and distribution of Aβ plaques must be inferred from in vitro pathological changes in brain tissue. In situ detection of Aβ plaques in live imaging is challenging because of the lack of adequate probes. Here we report the design of unimolecular quinoline-malononitrile-based Aβ probes, termed QMFluor integrative framework, that binds in vivo to Aβ plaques, making them detectable via near-infrared fluorescence imaging, magnetic resonance imaging, positron emission tomography and computed tomography. QMFluor probes are permeable to the blood-brain barrier, and, upon systematic injection, enable real-time magnetic resonance imaging and positron emission tomography-computed tomography imaging of the Aβ biodistribution in the hippocampus and cerebral cortex, and accurately differentiate the brains of living Alzheimer's disease mouse models from wild-type controls. We further demonstrate the ability of QMFluor probes to reach the brain after intravenous injection in a large animal model. This strategy expands the toolbox of probes for in vivo visualization of amyloids in Alzheimer's disease pathological analysis, drug screening and clinical applications.

Liraglutide Inhibits Autophagy to Ameliorate Post-Cardiac Arrest Brain Injury and Ferroptosis in Rats.

To investigate whether Liraglutide had a neuroprotective after cardiac arrest and return of spontaneous circulation (CA/ROSC) and explore its potential mechanisms. Adopting an 8-min asphyxial cardiac arrest model.Evaluate the neurological deficit score (NDS), observe pathological changes in hippocampal tissue with HE staining, and measure the expression level of proteins in hippocampal tissue with Western blot. Detection of hippocampal cell apoptosis using TUNEL (TdT-mediated dUTP Nick-End Labeling) method. Immunofluorescence staining was used to detect the expression of LC-3 in the hippocampus, and enzyme linked immunosorbent assay (ELISA) was used to detect the inflammatory factor TNF-α and IL-1β in serum and hippocampus. Autophagy and apoptosis were activated and the expressions of proteins reached significance at 24h after CA/ROSC. Moreover, rapamycin enhanced apoptosis, ferroptosis and aggravated neuro-pathological damage while 3-methyladenine reduced that. Furthermore, liraglutide treatment improved the 7-day survival rate and NDS, reduced histological signs of injury and inhibited apoptosis, ferroptosis and inflammatory cytokines released after cardiac arrest, and these effects were offset by autophagy agonist. Liraglutide could exert a protective role against post-cardiac arrest brain injury, which could be partially mediated by inhibiting autophagy and ferroptosis. Results clearly indicate that liraglutide may attenuate post-cardiac arrest brain injury (PCABI) by anti-apoptotic and anti-inflammatory via inhibiting autophagy and ferroptosis.

Electroacupuncture Inhibits Ferroptosis by Modulating Iron Metabolism and Oxidative Stress to Alleviate Cerebral Ischemia–Reperfusion Injury

Ischemic stroke (IS) is one of the leading causes of mortality and long-term disability worldwide. Electroacupuncture (EA) is commonly used in the treatment of IS, meaning that may reduce cerebral ischemia–reperfusion injury (CIRI). The middle cerebral artery occlusion/reperfusion (MCAO/R) rat models were created by the modified Zea Longa suture method. EA treatment was performed for 7 consecutive days at the acupoints Neiguan (PC6), Shuigou (GV26), and Sanyinjiao (SP6). The neurological function was assessed using the Zausinger six-point neurological deficiency score. The cerebral infarct volume was detected by 2,3,5-triphenyl tetrazolium chloride (TTC) staining. Hematoxylin and eosin (HE) staining was employed to observe the pathological changes in brain tissues. Prussian blue staining was employed to investigate iron deposition within the brain tissues. Transmission electron microscopy (TEM) was utilized to examine the morphological characteristics of mitochondria. Simultaneously, flow cytometry was utilized to detect the fluorescence intensity of reactive oxygen species (ROS). Assay kits were employed to measure the levels of Fe2+ and glutathione (GSH). Additionally, western blot (WB) and real-time quantitative polymerase chain reaction (RT-qPCR) assays were performed to evaluate the expression levels of proteins associated with ferroptosis. Compared with the MCAO/R group, both the MCAO/R + EA and MCAO/R + DFO groups exhibited significant improvements in neurological function following cerebral ischemia–reperfusion (CIR), attenuated the pathological brain tissue injury, and reduced the cerebral infarct volume and iron deposition in brain tissue. Furthermore, both the MCAO/R + EA and MCAO/R + DFO groups displayed a marked reduction in mitochondrial injury. There was a substantial decrease in Fe2+ and ROS levels, accompanied by a notable increase in GSH level and glutathione peroxidase 4 (GPX4) activity. Compared with the MCAO/R group, the levels of ferroportin1 (FPN1) protein and mRNA expression were significantly increased in the MCAO/R + EA and MCAO/R + DFO groups, and the expression levels of transferrin (TF), transferrin receptor 1 (TFR1), divalent metal transporter 1 (DMT1) protein and mRNA, as well as ferritin (FER) protein, were significantly decreased. EA inhibits ferroptosis by modulating iron metabolism and oxidative stress to alleviate CIRI, exerting neuroprotective effects.Graphical

Molecular mechanism of SH3GL3 recombinant protein and attenuates the acute lung inflammation in Klebsiella pneumonia rats by mollugin treatment by regulating STAT3/ROS signaling pathway.

Molecular mechanism of SH3GL3 recombinant protein and attenuates the acute lung inflammation in Klebsiella pneumonia rats by mollugin treatment by regulating STAT3/ROS signaling pathway.

Investigating the mechanism of action of Qianlie Jindan tablets in rats with chronic prostatitis using non-targeted metabolomics.

Investigating the mechanism of action of Qianlie Jindan tablets in rats with chronic prostatitis using non-targeted metabolomics.

Bazi Bushen Capsule Modulates Akkermansia muciniphila and Spermidine Metabolism to Attenuate Brain Aging in SAMP8 Mice.

Bazi Bushen Capsule Modulates Akkermansia muciniphila and Spermidine Metabolism to Attenuate Brain Aging in SAMP8 Mice.

Mechanism study of the effects of astragaloside IV and quercetin on idiopathic pulmonary fibrosis.

This study aimed to investigate the effects of astragaloside IV(AS-IV) and quercetin (QCT) on autophagic activity, pyroptosis, and epithelial-mesenchymal transdifferentiation (EMT) in the context of idiopathic pulmonary fibrosis (IPF), utilizing both in vivo and in vitro models. In the in vivo component of the research, C57BL/6J mice were subjected to bleomycin (BLM) modeling, followed by AS-IV + QCT intervention at low, medium, and high doses for 14 and 28days. Pathological changes in lung tissue were assessed through HE and Masson staining. Additionally, the expression levels of autophagy and pyroptosis-related proteins in serum and bronchoalveolar lavage fluid were examined via Western blot analysis. In the in vitro experiment, RAW264.7 macrophage cells were co-cultured with MLE-12 alveolar epithelial cells (3:1 ratio), implementing BLM and NLR family pyrin domain-containing protein (NLRP3) + BLM models to induce IPF. The effects of AS-IV and QCT on these cells were evaluated by electron microscopy to observe structural changes, while Western blot and ELISA were used to measure the expression of autophagy and pyroptosis-related proteins. Results showed that AS-IV and QCT significantly enhanced autophagic activity, evidenced by increased levels of LC3II and beclin-1 and decreased levels of P62. Additionally, both compounds reduced the expression of pyroptosis-related proteins (NLRP3, Caspase-1, IL-1β, and IL-18) and slowed the progression of EMT in alveolar epithelial cells. These findings propose that AS-IV and QCT inhibit the EMT process in IPF by activating autophagic mechanisms while suppressing pyroptosis, thereby underscoring their potential as innovative therapeutic strategies for IPF and highlighting the promising implications of herbal compounds in its prevention and treatment.

Periodontal tissue changes under chronic tobacco intoxication in an experimental model of gingival recession: a laser Doppler flowmetry study in rats

Background: At present, microcirculatory disturbances in organs and tissues have emerged as a critical issue in both experimental and clinical medicine, including periodontology. The findings presented in this article underscore the need for early detection of microcirculatory disorders in the periodontium under conditions of tobacco intoxication, using laser Doppler flowmetry. This diagnostic method, which records changes in microvascular blood flow by detecting signals from moving erythrocytes within vessels, provides a clear assessment of regional tissue perfusion. Aim: To evaluate periodontal changes in rats with gingival recession under conditions of chronic tobacco intoxication (CTI), using laser Doppler flowmetry (LDF). Methods: To experimentally validate the use of LDF for detecting periodontal tissue damage, microcirculation in the periodontium was assessed using the LDF analyzer LAKK-02, version 4 (NPP Lazma, Russia). The study included 75 adult male Wistar rats, which were divided into five groups: control; CTI; gingival recession; gingival recession elimination under continued CTI; and gingival recession elimination under CTI with a temporary cessation protocol. Results: LDF revealed progression of pathological changes in periodontal tissues under conditions of tobacco intoxication and gingival recession, as evidenced by a decrease in connective tissue cell density and epithelial layer thickness. Conclusion: Noninvasive LDF provides qualitative insights into the condition of the periodontal complex and enables early identification of tissue pathology, facilitating timely therapeutic intervention.

Technological Advancement in Diagnosis of Bovine Mastitis: An Overview

Mastitis caused by infectious pathogens is still considered a devastating condition of dairy animals affecting animal welfare as well as economically incurring huge losses to the dairy industry by means of decreased production performance and increased culling rates. The inflammation of a cow’s udder and mammary glands, known as bovine mastitis, is typically brought on by bacterial infections. The clinical and subclinical signs and symptoms of the disease serve as the foundation for regular diagnosis. This emphasizes how important it is to identify and quickly find etiological agents at the farm level; many advance diagnostic methods have been developed for this purpose such as infra-red thermography (IRT), proteomic based diagnosis, sequencing, nanotechnology based diagnosis, specific Immunoassays, sensor for mastitis detection, enzymatic biomarker,specific culture, polymerase chain reaction, micro-RNA based diagnosis, Recombinase polymerase amplification (RPA) and High resolution-melt analysis. Mastitis is multi-etiological complex disease as it is the outcome of interaction of various factors: the host, pathogens and the environment. The disease is characterized by physical, chemical and bacteriological changes in the milk and pathological changes in the glandular tissue of the udder. The global prevalence of clinical mastitis (CM) and subclinical mastitis (SCM) was 15% and 42%, respectively. Buffaloes are thought to be less prone to mastitis compare to cow. Improved milking hygiene, implementation of post-milking teat disinfection and maintenance of milking machinery are all general methods to avoid new cases of mastitis.

The cardioprotective effects of acteoside in myocardial ischemia reperfusion injury and the underlying mechanism

IntroductionWe observed the cardioprotective effects of Acteoside (AC) on myocardial ischemia reperfusion injury (MIRI) and discussed the possible mechanisms.MethodsBefore MIRI model was established successfully, AC was administrated to SD rats by gastric route for 7 d. Punctuate paw withdrawal threshold (PWT) was recorded to reflect the pain threshold. Blood samples were collected to measure the levels of oxidative stress, myocardial enzymes and Norepinephrine (NE). Hematoxylin and eosin (HE) staining was performed to observe the pathological changes of myocardial tissues. Apoptosis of myocardial cell was determined by transferase-mediated dUTP nick end labeling (TUNEL) assay, and the expressions of Bcl-2 and Bax were determined by Western blotting. Using network pharmacological analysis, the PI3K/Akt signaling pathway was screened to be associated with both AC and MIRI. Subsequently, the expressions of PI3K, p-Akt and caspase-3 were detected by immunochemistry in myocardial tissues.ResultsWe found that pre-administration of AC improved pain threshold and pathological change of myocardial structure caused by MIRI. AC reduced serum levels of myocardial enzymes and NE in MIRI. Compared with the Sham group, rats in MIRI group showed enhanced oxidative stress levels. These changes were partly reversed by AC. In addition, AC inhibited apoptosis, regulated the expression of apoptosis-related proteins. Immunochemistry analysis confirmed that AC increased the expressions of PI3K and p-Akt in myocardial tissue.ConclusionThe cardioprotective effects of AC in MIRI were related with pain alleviation, oxidative stress, apoptosis and sympathetic nerve activity inhibition, the PI3K/Akt signal pathway activation.Clinical trial numberNot applicable.

Senegenin ameliorates diabetic encephalopathy via promoting mitophagy and repressing NLRP3 inflammasome activation.

Diabetic encephalopathy (DE) remains a severe complication of diabetes in central nervous system with limited effective therapy. This study investigated the beneficial effect of senegenin on DE and its possible mechanisms. Type 2 diabetes mellitus mouse model and high-glucose (HG)-stimulated PC-12 cells were used as the in vivo and in vitro DE models. Learning and memory ability was evaluated by MWM test. Pathological changes in the brain tissues were determined by HE staining. Cell viability was detected by CCK-8. Mitochondrial membrane potential was measured by JC-1 probe. Target protein levels were assessed by Western blotting. Nucleotide-binding domain-like receptor protein 3 (NLRP3) expression was observed by immunofluorescent staining. Cognitive impairment and obvious pathological changes were found in DE mice, which were effectively attenuated by senegenin treatment. In addition, senegenin induced mitophagy and maintained homeostasis of mitochondrial dynamics to relieve mitochondrial dysfunction. Moreover, NLRP3 inflammation activation induced by DE was inhibited by senegenin. Finally, inhibition of mitophagy counteracted senegenin-mediated inactivation of NLRP3 inflammation and neuroprotection. Senegenin relieved diabetic encephalopathy via inducing mitophagy to inactivate NLRP3 inflammasome. Senegenin might be an effective therapy for treating DE.

Apigenin attenuates ischemia-reperfusion-induced pulmonary ferroptosis and fibrosis by activating the Nrf2/HO-1/GPX4 axis in mice.

Acute lung injury (ALI) is a major cause of morbidity and mortality after lung ischemia-reperfusion injury (LIRI). In recent years, pulmonary ferroptosis and its associated fibrosis have been recognized as important causes of LIRI. The purpose of this study is to investigate apigenin (APG) as a potential therapeutic target for treating LIRI-induced pulmonary ferroptosis and fibrosis. A rat model of LIRI was established and the rats were randomly divided into three groups, a sham group, a LIRI group, and an APG group. The pathological changes of the lung tissue were evaluated using hematoxylin-eosin staining and Masson's trichrome staining. Alterations in lung function were assessed using the pulmonary permeability index, myeloperoxidase, and wet-to-dry weight ratio. The pulmonary ferroptosis levels were evaluated by testing Fe2+, the ratio of reduced glutathione to oxidized glutathione disulfide, and malondialdehyde. Western blotting was performed to investigate the effect of APG on the expression of ferroptosis and fibrosis biomarkers in the lung tissues. The results show that APG pretreatment relieves LIRI-induced pulmonary pathological damage and functional abnormalities in rats. In addition, APG administration can significantly improve LIRI-induced pulmonary ferroptosis and fibrosis levels. However, using Nrf2 inhibitors to block the Nrf2/HO-1/GPX4 pathway significantly reversed these therapeutic effects. These findings suggest that APG protects against LIRI-induced ferroptosis and fibrosis of lung tissues via the activation of the Nrf2/HO-1/GPX4 axis.

Liensinine attenuates inflammatory response and oxidative stress by activation of Nrf2/HO- 1 signaling in L-NAME-induced gestational hypertension.

Pregnancy-induced hypertension (PIH) is a serious condition that can affect pregnant women after 20 weeks of gestation, which leads to preeclampsia, eclampsia, or even organ damage. Liensinine exhibits a diverse array of biological activities, encompassing anti-arrhythmic, anti-cancer, anti-hypertensive, and anti-pulmonary fibrotic properties. However, the role of Liensinine remains uncharacterized in PIH. Wistar rats were induced by L-NAME to establish the PIH model. The mean arterial pressure and urine protein were measured for hypertension evaluation. The reverse transcription quantitative PCR and Western blot analyses were used for mRNA and protein levels determination, respectively. In addition, H&E staining and TUNEL staining were performed to assess histological changes. Liensinine improved hypertensive symptoms of L-NAME-induced rats by decreasing mean arterial pressure. Besides, Liensinine ameliorated the pregnancy outcomes of L-NAME-induced rats. In addition, Liensinine suppressed inflammatory response and oxidative stress injury in PIH rats. Moreover, Liensinine promoted the release of growth factors including PIGF and VEGF in PIH rats. Furthermore, Liensinine improved pathological changes of placenta tissue and inhibited cell apoptosis. Mechanistically, Liensinine activates Nrf2/HO- 1 signaling by upregulating Nrf2 and HO- 1 protein levels. Liensinine attenuated inflammatory response and oxidative stress by activation of Nrf2/HO- 1 signaling in PIH.

Mechanism of 2,6-DMBQ attenuates airway inflammatory responses in asthmatic mice via the mTOR signaling pathway

To investigate the therapeutic effects and mechanisms of 2,6-dimethoxy-1,4-benzoquinone (2,6-DMBQ) in a mouse model of asthma. SPF-grade BALB/c mice were randomly divided into 7 groups (n=8 each group): normal control group, ovalbumin (OVA) group, dimethyl sulfoxide+corn oil group, budesonide (BUD) group, and low, medium, and high dose 2,6-DMBQ groups. An asthma mouse model was established by OVA induction, followed by corresponding drug interventions. Non-invasive lung function tests were performed to measure airway hyperresponsiveness, and enzyme-linked immunosorbent assay was used to determine levels of interleukin (IL)-17, IL-10, and serum immunoglobulin E in bronchoalveolar lavage fluid. A cell counter was employed to detect eosinophil counts in bronchoalveolar lavage fluid, while hematoxylin-eosin staining and periodic acid-Schiff staining were used to assess lung tissue pathological changes. Western blot was conducted to examine the expression of proteins related to the mammalian target of rapamycin pathway (p-AKT/AKT and p-p70S6K/p70S6K), and a fully automated biochemical analyzer was used to evaluate liver and kidney functions. Compared with the normal control group, the OVA group showed increased enhanced pause values, inflammation scores from hematoxylin-eosin staining, positive area from periodic acid-Schiff staining, percentage of eosinophils, IL-17/IL-10 ratio, serum immunoglobulin E levels, and relative expression levels of p-AKT/AKT and p-p70S6K/p70S6K (P<0.05). The BUD group and the medium and high dose 2,6-DMBQ groups exhibited decreased values for these indicators compared to the OVA group (P<0.05). 2,6-DMBQ can inhibit the mTOR pathway to alleviate airway inflammation in asthmatic mice, possibly by mitigating the imbalance between Th17 and regulatory T cells.

Anti-cancer effects of carnosol in DMBA-induced oral experimental carcinogenesis by oncogenic signaling pathways on in vivo and in silico study.

The most prevalent malignant tumor in the oral cavity, accounting for more than 90% of all oral malignancies, is oral squamous cell carcinoma (OSCC). Therefore, detection or prevention of malignant transformation remains a viable target for the future. Carnosol is a compound derived from rosemary that contains both antioxidant and anti-carcinogens. This study examined the defensive properties of carnosol in DMBA-induced oral carcinogenesis. We have developed the computational based docking analysis to predict the binding affinity and interaction of carnosol with inflammatory and pro-apoptotic proteins. Carnosol was the most potential bioactive compound shows strong binding affinity to low binding energy to bind above the proteins. Following this, we created a hamster model to study buccal pouch carcinogenesis induced by DMBA and assessed buccal tissues using histopathological, biochemical, and western blotting. Carnosol treatment effectively reduced DMBA-induced pathological changes in buccal tissues: Altered detoxification, increased antioxidant levels, and reduced lipid peroxidation enzymes levels. We then examined the impact of carnosol intervention on the modulation of the levels of inflammatory factors and pro-apoptotic markers in oral carcinogenesis. Binding energy was studied between the carnosol between the inflammatory (NF-κB and COX-2) and apoptotic (Bax, caspase-3, and caspase-9) proteins using molecular docking. Our findings suggest that carnosol enhances antioxidant and detoxification levels, potentially prevents oral carcinogenesis by modifying the inflammatory and pro-apoptotic signaling pathways, and acts as an anti-cancer agent.

MiR‐29 inhibits endothelial‐to‐mesenchymal transition in pulmonary hypertension of the newborn by regulating LRP6

AbstractPulmonary hypertension of the newborn (PHN) is a common pulmonary vascular disease in newborns, affecting the prognosis of affected infants and even leading to death. Currently, there is still no specific targeted prevention and treatment program available. In recent years, research on the regulatory mechanism of endothelial‐to‐mesenchymal transition (EndMT) has become a hot topic, with the interplay between miRNAs and the Wnt signaling pathway playing an important role. MiR‐29 is highly expressed in distal pulmonary arteriolar smooth muscle cells and endothelial cells. In miR‐29 gene knockout mice, pathological changes in lung tissue can be observed, indicating an obstruction in the maturation of smooth muscle cells in the distal pulmonary arterioles. LRP6 is an important Wnt co‐receptor in the Wnt signaling pathway, and the Targetscan website predicts a binding site between miR‐29 and LRP6. Therefore, our studies establish a role for decreased miR29a in the endothelial mesenchymal transition through activation of the LRP6‐Wnt signaling pathway in neonatal hypoxia‐mediated PAH. By generating hypoxic newborn rat models of pulmonary artery hypertension and hypoxic injury models of pulmonary vascular endothelial cells, we observed the presence of EndMT in the model group, as well as the activation of the LRP6 and Wnt/β‐catenin signaling pathways and the differential expression of the miR‐29 family, particularly miR‐29a. Subsequently, We used cell transfection technology to overexpress/knock down miR‐29a and LRP6, respectively, to observe changes in EndMT‐related indicators and successfully found that miR‐29a and LRP6 can negatively and positively regulate the occurrence of EndMT, respectively. Finally, the dual‐luciferase reporter gene assay confirmed that LRP6 can directly bind to miR‐29a‐3p. These findings provide experimental evidence of the potential of miR‐29 as a novel target for the prevention and treatment of PHN.

Platycodon grandiflorum exosome-like nanoparticles: the material basis of fresh platycodon grandiflorum optimality and its mechanism in regulating acute lung injury

BackgroundAcute lung injury (ALI) is a severe respiratory disease accompanied by diffuse inflammatory responses induced by various clinical causes. Many fresh medicinal plants have shown better efficacy than their dried forms in preventing and treating diseases like inflammation. As a classical Chinese herb, platycodon grandiflorum (PG) has been demonstrated effective in treating pneumonia, but most of previous studies focused on the efficacy of processed or dried PG formats, while the specific benefits of its fresh form are still underexplored. Exosome-like nanoparticles derived from medicinal plants are expected to point out an important direction for exploring the material basis and mechanism of this fresh herbal medicine.ResultsThe fresh form of PG could effectively improve ALI induced by lipopolysaccharide (LPS), relieve lung histopathological injury and weight loss, and reduce levels of inflammatory factors in mice, exhibiting better efficacy than dried PG in the treatment of ALI. Further extraction and purification of PG exosome-like nanoparticles (PGLNs) demonstrated that PGLNs had good biocompatibility, with characteristics consistent with general exosome-like nanoparticles. Besides, proteomic analysis indicated that PGLNs were rich in a variety of proteins. Animal experiments showed that PGLNs improved the pathological changes in LPS-induced lung tissues, inhibited the expression of inflammatory factors and promoted the expression of anti-inflammatory factors, and exerted a regulatory effect on the polarization of lung macrophages. Cell experiments further confirmed that PGLNs could be effectively taken up by RAW264.7 cells and repolarize M1 macrophages into M2 type, therefore reducing the secretion of harmful cytokines. Moreover, non-targeted metabolomics analysis reveals that PGLNs reduce inflammation and control macrophage polarization in a manner closely linked to pathways including glycolysis and lipid metabolism, highlighting a potential mechanism by which PGLNs protect the lungs from inflammatory damage like ALI.ConclusionFresh PG has better anti-inflammatory and repair effects than its dried form. As one of the most effective active substances in fresh PG, PGLNs may regulate macrophage inflammation and polarization by regulating metabolic pathways including lipid metabolism and glycolysis, so as to reduce inflammation and repair lung injury.

Evaluation of Immunopharmacological efficacy of live Leishmania donovani overexpressing Ld_ζ1domain for protection against experimental human visceral Leishmaniasis.

Evaluation of Immunopharmacological efficacy of live Leishmania donovani overexpressing Ld_ζ1domain for protection against experimental human visceral Leishmaniasis.

Ermiao San attenuating rheumatoid arthritis via PI3K/AKT/mTOR signaling activate HIF-1α induced glycolysis.

Ermiao San attenuating rheumatoid arthritis via PI3K/AKT/mTOR signaling activate HIF-1α induced glycolysis.