Fatty acid oxidation is a major metabolic pathway responsible for fatty acid breakdown and energy production. Carnitine palmitoyltransferase 1A (CPT1A), the rate-limiting enzyme in this process, catalyzes the conversion of acyl-coenzyme A into acyl-carnitine, enabling mitochondrial transport for oxidative metabolism. Emerging evidence indicates that dysregulated CPT1A contributes to metabolic disorders and cancer progression by driving metabolic reprogramming, modulating oxidative stress, and regulating protein modifications, including histone acetylation and lysine succinylation. Colorectal cancer (CRC), one of the leading causes of cancer-related mortality worldwide, has recently been linked to aberrant CPT1A activity. Studies demonstrate that CPT1A promotes CRC progression by regulating oncogenic signaling pathways, enhancing cancer stemness, supporting tumor proliferation and metastasis, and shaping the tumor microenvironment. Increasing evidence suggests that targeting CPT1A may be a promising therapeutic strategy for CRC. In this review, we summarize the biological functions of CPT1A, discuss its mechanistic role in CRC progression, and highlight its emerging potential as a metabolic and therapeutic target in CRC.

AbstractHematopoietic stem cell transplantation (HSCT) is a highly effective therapy for malignant blood illnesses that pose a high risk, as well as diseases that are at risk due to other variables, such as genetics. However, the prevalence of graft-versus-host disease (GVHD) has impeded its widespread use. Ensuring the stability of microbial varieties and associated metabolites is crucial for supporting metabolic processes, preventing pathogen intrusion, and modulating the immune system. Consequently, it significantly affects the overall well-being and susceptibility of the host to disease. Patients undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT) may experience a disruption in the balance between the immune system and gut bacteria when treated with medicines and foreign cells. This can lead to secondary intestinal inflammation and GVHD. Thus, GM is both a reliable indicator of post-transplant mortality and a means of enhancing GVHD prevention and treatment after allo-HSCT. This can be achieved through various strategies, including nutritional support, probiotics, selective use of antibiotics, and fecal microbiota transplantation (FMT) to target gut microbes. This review examines research advancements and the practical use of intestinal bacteria in GVHD following allo-HSCT. These findings may offer novel insights into the prevention and treatment of GVHD after allo-HSCT.

In this study, we established a mouse colitis model using DSS to investigate the impact of curcumin on gut injury, the intestinal microbiota, and fecal metabolites. The findings indicated that curcumin effectively mitigated weight loss and colon shortening caused by colitis, enhanced the expression of anti-inflammatory factor IL-10 mRNA (p < 0.05), and suppressed the expression of pro-inflammatory factors (IL-1β, IL-6, and TNF-α mRNA; p < 0.05). 16S rDNA sequencing analysis showed that in the CUR group, compared to the NC and DSS groups, the abundances of Bacteroides, Lachnospiraceae NK4A136, and Ruminococcaceae UGC 014 significantly increased, while that of Lactobacillus markedly decreased. Additionally, compared with the DSS group, the CUR group demonstrated a significant decrease in levels of metabolites associated with nucleic acid and fat metabolism, including xanthosine, isocitric acid, and D-xylose. Conversely, levels of metabolites of curcumin, such as demethoxycurcumin and tetrahydrocurcumin, were significantly elevated in the CUR group. Curcumin appears to offer protection against mouse colitis by potentially enhancing the composition of the gut microbiota and regulating metabolic and inflammatory processes through its metabolites.

The flowers of Abelmoschus manihot (L.) Medic are commonly used in clinical practice in China to cure forms of chronic kidney disease. Despite a long history of traditional use, the flowers obtained by different drying technologies have never been fully chemically characterized, and the ranges of constituents between different drying methods have not been comprehensively reported. To establish a quality control and chemical characterization method, a total of 14 batches of samples corresponding to 14 postharvest treatments were studied. Seven flavonoids were quantified using a HPLC-PDA method. The method was validated in terms of linearity (r > 0.999), precision (intra- and inter-day: 0.7-1.4 %), accuracy (99.90-100.7 %), detection limit (0.34-0.46 mu g/mL) and quantification limit (1.15-1.52 mu g/mL). The contents of total flavonoids in manihot flowers were as follows in descending order: Infrared Drying (50.96 mg/g) > Microwave Drying (41.84 mg/g) approximate to Hot-air Drying (39.58 mg/ g) approximate to Fresh (39.35 mg/g) approximate to Primary Drying (38.95 mg/g). Principal component analysis showed that samples processed with Fresh, Primary Drying, and the investigated three modern drying methods were well classified into three domains, indicating an important difference between drying methods. For the purpose of saving the flavonoids contents, infrared drying under 80-100 degrees C would be most acceptable. Furthermore, using UHPLC QExactive Orbitrap MS data with targeted and non-targeted approaches, 28 compounds were identified in Abelmoschus manihot samples. Flavonoids were the main group of compounds found in Abelmoschus manihot flowers. The study could provide the scientific evidence for the selection and optimization of appropriate drying method for manihot flowers, and also provide the reference for the formation of generic primary drying processing technology for medicinal flowers containing flavonoids.

Inflammatory bowel disease (IBD), a chronic immune disorder, has increasing global incidence and poor treatment outcome. Abnormal macrophage function is implicated in the pathophysiology of IBD. In this study, we investigated the mechanism by which human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) inhibit inflammation in IBD mouse and macrophage inflammation models. We established a dextran sodium sulfate (DSS)-induce BALB/c mice model of IBD and treated with hucMSC-Ex via tail vein to evaluate their repair effect on IBD mice. An in vitro macrophage inflammation model was established using lipopolysaccharide (LPS) and Nigericin (Nig) by stimulating mouse macrophage RAW264.7 and human myeloid leukemia mononuclear (THP-1) cells to assess the repair effect of hucMSC-Ex on macrophage inflammation. EX 527, an effective inhibitor of silent information regulator of transcription 1 (SIRT1), was employed in both the in vivo and in vitro models to explore the effect of hucMSC-Ex on the SIRT1-FXR (farnesoid X receptor) pathway in macrophages during the attenuation of inflammation. HucMSC-Ex effectively inhibited inflammation in both the in vivo and in vitro models by up-regulating the expressions of SIRT1 and FXR, which reduced the acetylation level of FXR and inhibited the activation of NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome. The addition of EX 527 further proved that hucMSC-Ex can reduce the acetylation of FXR by activating the SIRT1-FXR pathway, and the decrease of FXR acetylation was directly related to the inhibition of the activity of the NLRP3 inflammasome. HucMSC-Ex alleviates IBD by reducing the acetylation level of FXR through activating the SIRT1-FXR pathway in macrophages and directly negatively regulating the activation of NLRP3 inflammasomes, thus inhibiting the occurrence of the inflammatory process.

Inflammatory bowel disease (IBD) and colorectal cancer (CRC), as two of the major human intestinal diseases, provide challenges for the medical field. Suppressor of cytokine signaling 3 (SOCS3), a protein molecule that negatively regulates cytokine signaling through multiple pathways, is involved in the regulation of various inflammatory diseases and tumors. In IBD, SOCS3 acts on a variety of cells to repair mucosal damage and balance the immune response, including epithelial cells, macrophages, dendritic cells, neutrophils, and T cells. In CRC, SOCS3 is inextricably linked to tumor cell proliferation, invasion, metastasis, and drug resistance. Therefore, it is crucial to systematically investigate the pathogenic involvement of SOCS3 in IBD and CRC. This article reviews the mechanisms and pathways by which SOCS3 is involved in the inhibition of IBD and the mitigation of CRC, and details the therapeutic options for targeting SOCS3.

Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is a complex disorder with an unknown cause. However, the dysbiosis of the gut microbiome has been found to play a role in IBD etiology, including exacerbated immune responses and defective intestinal barrier integrity. The gut microbiome can also be a potential biomarker for several diseases, including IBD. Currently, conventional treatments targeting pro-inflammatory cytokines and pathways in IBD-associated dysbiosis do not yield effective results. Other therapies that directly target the dysbiotic microbiome for effective outcomes are emerging. We review the role of the gut microbiome in health and IBD and its potential as a diagnostic, prognostic, and therapeutic target for IBD. This review also explores emerging therapeutic advancements that target gut microbiome-associated alterations in IBD, such as nanoparticle or encapsulation delivery, fecal microbiota transplantation, nutritional therapies, microbiome/probiotic engineering, phage therapy, mesenchymal stem cells (MSCs), gut proteins, and herbal formulas.

Objective: Patients with chronic cervicitis are known to have an increased risk of infection with human papillomavirus (HPV), which is the primary cause of cervical cancer. Inhibition of cervical inflammation may reduce the risk of cervical cancer. This study investigated how human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) attenuated the lipopolysaccharide (LPS)-induced cervical inflammation. Methods: Human uterine squamous carcinoma (SiHa) cells were induced with LPS to construct an inflammatory model and treated with hucMSC-Ex. The expression levels of tumor necrosis factor alpha (TNF-alpha), and interleukins (IL)-1(3, IL-6, IL-10 were analyzed by qRT-PCR. Western blot was used to detect the protein expression levels of cyclooxygenase-2 (COX-2) and proliferating cell nuclear antigen (PCNA) in cells, and CCK8 was used to examine cell proliferation, so as to explore the relieving effect of hucMSC-Ex on cell inflammation. The expression of epithelial-mesenchymal transition (EMT) markers in SiHa cells was also assessed by qRT-PCR and western blot to determine the effect of hucMSC-Ex on inflammation. Moreover, clinical cervical smears were collected to detect the expression of EMT markers in clinical exfoliated cell samples by immunofluorescence. Results: HucMSC-Ex treatment significantly reduced the expression of pro-inflammatory cytokines, such as TNF-alpha, IL-1(3, and IL-6 in the LPS-induced inflammation model, while increasing the level of anti-inflammatory cytokines, including IL-10, to reduce inflammation. HucMSC-Ex increased the expression level of epithelial markers (such as E-cadherin) while it decreased the expression of interstitial markers (such as N-cadherin), suggesting it inhibits EMT. Conclusions: Our results support that hucMSC-Ex alleviates LPS-induced cervical inflammation, possibly by inhibition of EMT.

BACKGROUND:Inflammatory bowel disease (IBD) is a chronic inflammatory disease that poses challenges in terms of treatment. The precise mechanism underlying the role of human umbilical cord mesenchymal stem cell-derived exosome (HucMSC-Ex) in the inflammatory repair process of IBD remains elusive. Mucosal mast cells accumulate within the intestinal tract and exert regulatory functions in IBD, thus presenting a novel target for addressing this intestinal disease. METHODS:A mouse model of Dextran Sulfate Sodium (DSS)-induced colitis was established and hucMSC-Ex were administered to investigate their impact on the regulation of intestinal mast cells. An in vitro co-culture model using the human clonal colorectal adenocarcinoma cell line (Caco-2) and human mast cell line (LAD2) was also established for further exploration of the effect of hucMSC-Ex. RESULTS:We observed the accumulation of mast cells in the intestines of patients with IBD as well as mice. In colitis mice, there was an upregulation of mast cell-related tryptase, interleukin-33 (IL-33), and suppression of tumorigenicity 2 receptor (ST2 or IL1RL1), and the function of the intestinal mucosal barrier related to intestinal tight junction protein was weakened. HucMSC-Ex treatment significantly reduced mast cell infiltration and intestinal damage. In the co-culture model, a substantial number of mast cells interact with the epithelial barrier, triggering activation of the IL-33/IL1RL1 (ST2) pathway and subsequent release of inflammatory factors and trypsin. This disruption leads to aberrant expression of tight junction proteins, which can be alleviated by supplementation with hucMSC-Ex. CONCLUSION:Our results suggest that hucMSC-Ex may reduce the release of mast cell mediators via the IL-33/IL1RL1 (ST2) axis, thereby mitigating its detrimental effects on intestinal barrier function.

为了提高全国职业院校技能大赛化学实验技术赛项硫酸亚铁铵产品的产率和纯度,通过L9(3)4 正交试验优选制备工艺.结果显示,制备工艺影响因素依次为铁粉与硫酸物质的量比(A)＞反应温度(C)＞铁粉与硫酸铵物质的量比(B),制备最佳工艺为A3 B2 C3,即n(铁粉)∶ n(硫酸)为1 ∶ 1.5,n(铁粉)∶ n(硫酸铵)为1 ∶ 1.05,反应温度为85℃.该工艺合理,所制备硫酸亚铁铵的产率和纯度较高.

In the 2022 Jiangsu vocational skills competition “Chemical Experiment Technology” item, sulfosalicylic acid spectrophotometry or 1,10-phenanthroline spectrophotometry were used to determine the content of iron in samples. During the experiment, the cleanliness of glassware, the design of standard curve, the preparation of the solution to be tested, and the time of solution color development all affect the experimental results. In view of the above factors, suggestions for improvement are put forward to improve the accuracy of the determination results.

Farnesoid-X receptor (FXR), as a nuclear receptor activated by bile acids, is a vital molecule involved in bile acid metabolism. Due to its expression in immune cells, FXR has a significant effect on the function of immune cells and the release of chemokines when immune cells sense changes in bile acids. In addition to its regulation by ligands, FXR is also controlled by post-translational modification (PTM) activities such as acetylation, SUMOylation, and methylation. Due to the high expression of FXR in the liver and intestine, it significantly influences intestinal homeostasis under the action of enterohepatic circulation. Thus, FXR protects the intestinal barrier, resists bacterial infection, reduces oxidative stress, inhibits inflammatory reactions, and also acts as a tumor suppressor to impair the multiplication and invasion of tumor cells. These potentials provide new perspectives on the treatment of intestinal conditions, including inflammatory bowel disease (IBD) and its associated colorectal cancer (CRC). Moreover, FXR agonists on the market have certain organizational heterogeneity and may be used in combination with other drugs to achieve a greater therapeutic effect. This review summarizes current data on the role of FXR in bile acid metabolism, regulation of immune cells, and effects of the PTM of FXR. The functions of FXR in intestinal homeostasis and potential application in the treatment of IBD and CRC are discussed.

Short-chain fatty acids (SCFAs) are important anti-inflammatory metabolites of intestinal flora. Oxidized low-density lipoprotein (ox-LDL)-induced macrophage activation is critical for the formation of atherosclerosis plaque. However, the association between SCFAs and ox-LDL-induced macrophage activation with respect to the formation of atherosclerosis plaque has not yet been elucidated. The present study investigated whether SCFAs (sodium acetate, sodium propionate, and sodium butyrate) can affect ox-LDL-induced macrophage activation and potential signaling pathways via regulation of the expression of the NLRP3/Caspase-1 pathway. Using human monocyte-macrophage (THP-1) cells as a model system, it was observed that ox-LDL not only induced cell inflammatory injury but also activated the NLRP3/Caspase-1 pathway. The exogenous supplementation of three SCFAs could significantly inhibit cell inflammatory injury induced by ox-LDL. Moreover, three SCFAs decreased the expression of IL-1β and TNF-α via the inactivation of the NLRP3/Caspase-1 pathway induced by ox-LDL. Furthermore, three SCFAs affected cellular metabolism in ox-LDL-induced macrophages, as detected by untargeted metabolomics analysis. The results of the present study indicated that three SCFAs inhibited ox-LDL-induced cell inflammatory injury by blocking the NLRP3/Caspase-1 pathway, thereby improving cellular metabolism. These findings may provide novel insights into the role of SCFA intervention in the progression of atherosclerotic plaque formation.

Gastrointestinal tumours are the most common solid tumours, with a poor prognosis and remain a major challenge in cancer treatment. Mesenchymal stem cells (MSC) are multipotent stromal cells with the potential to differentiate into multiple cell types. Several studies have shown that MSC-derived exosomes have become essential regulators of intercellular communication in a variety of physiological and pathological processes. Notably, MSC-derived exosomes support or inhibit tumour progression in different cancers through the delivery of proteins, RNA, DNA, and bioactive lipids. Herein, we summarise current advances in MSC-derived exosomes in cancer research, with particular reference to their role in gastrointestinal tumour development. MSC-derived exosomes are expected to be a novel potential strategy for the treatment of gastrointestinal cancers.

Inflammatory bowel disease (IBD), a chronic gut immune dysregulation and dysbiosis condition is rapidly increasing in global incidence. Regardless, there is a lack of ideal diagnostic markers, while conventional treatment provides scarce desired results, thus, the exploration for better options. Changes in the gut microbial composition and metabolites either lead to or are caused by the immune dysregulation that characterizes IBD. This study examined the fecal metagenomics and metabolomic changes in IBD patients. A total of 30 fecal samples were collected from 15 IBD patients and 15 healthy controls for 16S rDNA gene sequencing and UHPLC/Q-TOF-MS detection of metabolomics. Results showed that there was a severe perturbation of gut bacteria community composition, diversity, metabolites, and associated functions and metabolic pathways in IBD. This included a significantly decreased abundance of Bacteroidetes and Firmicutes, increased disease-associated phyla such as Proteobacteria and Actinobacteria, and increased Escherichiacoli and Klebsiellapneumoniae in IBD. A total of 3146 metabolites were detected out of which 135 were differentially expressed between IBD and controls. Metabolites with high sensitivity and specificity in differentiating IBD from healthy individuals included 6,7,4 '-trihydroxyisoflavone and thyroxine 4 '-o-.beta.-d-glucuronide (AUC = 0.92), normorphine and salvinorin a (AUC = 0.90), and trichostachine (AUC = 0.91). Moreover, the IBD group had significantly affected pathways including primary bile acid biosynthesis, vitamin digestion and absorption, and carbohydrate metabolism. This study reveals that the combined evaluation of metabolites and fecal microbiome can be useful to discriminate between healthy subjects and IBD patients and consequently serve as therapeutic and diagnostic targets.

As an intracellular pattern recognition receptor (PPR), the nucleotide-binding oligomerization domain-containing protein 2 (NOD2) triggers a cascade of immune responses. Previous studies of NOD2 regarding inflammatory bowel disease (IBD) mainly focused on the relevance of NOD2 mutations and loss within the disease onset and progression. With increasing research, more studies are exploring other functional roles and clinical applications of NOD2. In this review, we discuss the role of NOD2 in intestinal immune response and microbiota modulation in IBD and explore its clinical potential as a therapeutic target for IBD.

人体解剖学是医学教育的基石,为学习其他医学课程奠定必要的形态学基础.由于解剖学专业术语众多,人体形态结构复杂,内容枯燥乏味,传统教学方式难以取得良好的教学效果.近年来,新型教学方式发展迅速,促成人体解剖学教学在内容和方法上发生重大变化,为其教学改革提供了新思路.通过查阅近年发表的文献,重点围绕PBL教学法、病例分析教学法、混合式教学法、微课等几种典型的新型教学方式的特点及其在人体解剖学教学中的应用进行综述.

采用高脂饲料、腹腔注射链脲佐菌素(STZ)、高脂饲料+腹腔注射STZ等3种方法分别制备2型糖尿病小鼠模型,通过检测小鼠血糖水平和糖化血红蛋白(HbA1c)水平,评估所建模型是否成功.高脂饲料组小鼠第7周时血糖水平显著升高,而HbA1c水平与正常对照组无差异;腹腔注射STZ组小鼠血糖水平仅一过性升高后即恢复正常,HbA1c水平与正常对照组无差异;高脂饲料+腹腔注射STZ组小鼠第2周起血糖水平明显高于正常对照组,第3周起HbA1c水平明显高于正常对照组,随后逐渐升高,并维持高水平.采用高脂饲料+腹腔注射STZ法构建2型糖尿病小鼠模型具有省时、简便、经济等优点.

肠道微生物种群是人体最大的共生生态系统,在维持肠道生态平衡中发挥着重要作用.肠道微生态失衡的本质是共生微生物和致病微生物之间的失衡.大量研究表明,肠道内的各种共生微生物是保障肠黏膜免疫系统成熟所不可或缺的,而致病微生物的存在会引起各种免疫功能紊乱,最终导致疾病发生.另一方面,肠道菌群中细菌的种类和丰度也受到肠黏膜免疫系统的监视和影响,炎症状态下肠道微生态的平衡将被打破,导致多种肠道疾病发生.综述了近年来肠道菌群与肠黏膜免疫系统之间相互作用的研究进展.

The overactivation of macrophages causes chronic inflammatory diseases. Short-chain fatty acids (SCFAs), potential drugs for clinical treatment, are modulators of macrophage inflammatory reaction. Therefore, the modulation of macrophage-mediated cell activity is expected to become a new therapeutic strategy for inflammatory diseases caused by Mycoplasma pneumoniae. In this study, 2 kinds of SCFAs (propionate and butyrate) were found to have anti-inflammatory effects in M. pneumoniae-stimulated THP-1 cells inflammatory. They inhibited the expressions of IL-4, IL-6, ROS, and NLRP3 inflammasome, while enhancing the expressions of IL-10 and IFN-γ. Our study revealed these 2 agents to repress transcriptional activities of NF-κB, which are important modulators of inflammation. Meanwhile, SCFAs can significantly enhance the autophagy induced by M. pneumoniae. Considering that SCFAs have few side effects, they might be the promising adjuvant therapy for the prevention and/or treatment of various inflammatory diseases.