Significant causes of morbidity in veterinary medicine are tumourigenic diseases and pathogenic infections, which pose significant threats to animal health. Traditional methods for treating tumours and bacterial infections primarily involve chemotherapy and antibiotic therapy, both of which are associated with drug resistance and adverse effects. Photodynamic therapy (PDT) is gaining increasing interest in veterinary clinical practice because of its distinctive benefits such as spatiotemporal selectivity, low toxicity, fewer negative effects, and reduced risk of drug resistance. This review summarises the fundamental principles of PDT and its applications in combating tumours and microbial infections in veterinary practice involving companion animals, livestock, wildlife, and reptiles. It is worth noting that the existing clinical evidence is limited by very small sample sizes and the absence of comparator groups; however, these studies have provided a preliminary theoretical foundation and technical reference for further clinical development of PDT. Moreover, the opportunities and challenges associated with PDT in veterinary clinical practice are discussed herein.

Glycolipid metabolic diseases represent a group of disorders that arise from dysregulated metabolism of carbohydrates and lipids in livestock. With advancements in the farming industry, the incidence of these metabolic disorders in livestock has progressively increased, posing significant threats to animal health and undermining the economic viability of farming operations. In recent years, considerable attention has been directed toward the role of probiotics derived from gut microbiota in regulating glycolipid metabolism. Gut microbiota confer beneficial effects on glycolipid metabolism through various mechanisms, including enhancement of intestinal microecology, reduction of insulin resistance, regulation of lipid metabolism, production of short-chain fatty acids (SCFAs), and exertion of anti-inflammatory effects. However, the mechanisms underlying the actions of gut microbiota on glycolipid metabolism are complex. This review aims to summarize the mechanisms by which gut microbiota influence glycolipid metabolism in livestock and to explore their potential applications in the prevention, treatment, and management of glycolipid metabolic disorders. Consequently, this review provides new insights and a scientific basis for advancing research and developing strategies to address glycolipid metabolic diseases in livestock, particularly in bovine species.

Giardia duodenalis is a protozoan parasite responsible for waterborne diarrheal diseases in humans and animals worldwide. TLR4 is a key pattern recognition receptor of the innate immune system, and MHC-II bridges innate and adaptive responses, while role of these receptors in the activation of macrophages by G. duodenalis still needs further investigation. This study confirmed knockdown efficiency using RT-qPCR and western blotting then employed multiple molecular and cellular assays to investigate the functions of TLR4 and MHC-II in RAW264.7 macrophages during defense against G. duodenalis. Results showed that the significant upregulation of proinflammatory cytokines (e.g., 5.18-fold increase in IL6 expression) and marked activation of NF-kappa B pathways (marked enhancement of p65 fluorescence in the cell nucleus) in macrophages following G. duodenalis infection were dependent on TLR4, as demonstrated by their attenuation after TLR4 knockdown. Interestingly, we also observed that the knockdown of MHC-II produced similar results, and the elevated expression of MHC-II in macrophages induced by G. duodenalis was inhibited by the interference of class II transactivating factor (CIITA). Overall, CIITA/MHC-II/NF-kappa B pathway is critical for full activation of TLR4mediated innate immune response in macrophage initiated by G. duodenalis, which elaborated the innate immune network in the interaction between G. duodenalis and macrophages, holds significant implications for the immunotherapeutic strategies targeting Giardiasis.

BACKGROUND:The size of fat globules in milk, which is influenced mainly by the size of lipid droplets (LDs) in bovine mammary epithelial cells, affects the quality of the milk. The present study aimed to explore how lipophagy affected the catabolism of LDs in bovine mammary epithelial cells. RESULTS:Lipophagy was initiated by 24 h of starvation with serum-free culture medium. Compared with those in the control group (CT), the level of intracellular triglycerides and xanthine dehydrogenase (XDH) protein were lower, whereas the expression of perilipin 2 (PLIN2), peroxisome proliferator-activated receptor gamma (PPAR γ) and sterol regulatory element-binding protein 1 (SREBP1) was greater in response to starvation. The number of LDs was lower, whereas the average diameter of LDs and the distribution of large LDs (diameter > 3 μm) was greater in response to starvation. Inhibition of the lipophagic flux induced the accumulation of small LDs (diameter < 1 μm). Starvation enhanced the expression of adipose triglyceride lipase (ATGL), the inhibition of which increased average diameter of LDs and the accumulation of large LDs. Furthermore, colocalization of ATGL and large LDs was observed in cells subjected to starvation. Inhibition of lysosomal acid lipase decreased the size of LDs, and the colocalization of small LDs and autolysosomes was also observed in bovine mammary epithelial cells subjected to starvation. CONCLUSION:The results of the present study suggested that nutrient deficiency induced the formation of autophagosomes, which selectively delivered small lipid droplets to lysosomes for degradation and affected the catabolism of triglycerides in bovine epithelial cells. © 2025 Society of Chemical Industry.

The present study aimed to combine Portulaca oleracea L with PD to compose a new formula supplemented PD (SPD), and evaluate its effect on ulcerative colitis (UC). The UC mouse model was obtained by supplementing 3.5% dextran sulfate sodium salt (DSS) orally. Subsequently, the mice were treated with PBS, sulfasalazine, high dose SPD, medium dose SPD or low dose SPD. Morphological analysis, RT-qPCR, ELISA assay, LC-MS/MS analysis and 16s rRNA sequencing were conducted to evaluate the effect of SPD on UC. DSS treatment resulted in the decreased body weight and increased DAI value of the mice, while SPD mitigated the changes of body weight and DAI value induced by UC. SPD attenuated the proinflammatory response induced by UC by down regulating the expression of proinflammatory cytokines, and alleviated the oxidative stress in the gut of the mice with UC by downregulating the MDA level and enhancing the activity of antioxidant enzymes. Additionally, SPD also enhanced the transcription of MUC2 and Occludin which were inhibited by UC. Furthermore, DSS induced the dysbiosis of the colonic microbiota and relative abundance of the Akkermansia at genus level was higher in UC group whereas treatment with high-dose SPD restored its abundance to levels comparable to the control group. SPD demonstrated therapeutic effects on DSS-induced UC of the mice by attenuating the proinflammatory response, enhancing the antioxidant ability and key molecules related with barrier function, and modifying the gut microbiota, thereby providing a potential strategy for the treatment of ulcerative colitis.

Non-alcoholic fatty liver disease (NAFLD) is a clinicopathological syndrome characterized by hepatic steatosis associated with insulin resistance, oxidative stress, inflammatory responses, and other factors. A precise pathogenesis of NAFLD remains unclear. Although it has emerged as a global health burden, current therapeutic options for example, probiotics, prebiotics, synbiotics and fecal microbiota transplantation (FMT) have shown promising but varied efficacy. The use of traditional Chinese medicine (TCM) in NAFLD patients, has gained growing attention for its multi-targeted regulatory properties and the beneficial impacts of several natural product-formulations on gut microbiota, lipid metabolism and hepatic health. This article highlights the role of gut microbiota dysbiosis in the pathogenesis of NAFLD and explores the therapeutic strategies emphasizing the need of personalized multimodal approaches and robust clinical trials to validate these interventions.

Neonatal calves exhibit heightened susceptibility to infections caused by various gut microbiota, primarily due to their immature gastrointestinal barrier functions and underdeveloped immune systems during the pre-weaning period. Calf diarrhea poses a significant risk to the health of juvenile ruminants and can result in substantial financial losses within the livestock sector. Therefore, diarrhea is a significant disease that requires improved management practices and preventive measures in cattle rearing. Antibiotics are commonly administered to combat diarrhea and promote calf growth. However, their misuse has led to increased bacterial resistance and higher levels of antibiotic residues in meat. Consequently, finding advanced and alternative ways to treat newborn calf diarrhea for enhanced livestock production and public health is a significant challenge. Probiotic administration can offer significant advantages such as improving the internal microenvironment of the gut and enhancing the host's immune response, thereby reducing the likelihood of gastrointestinal diseases. Additionally, probiotic supplements have been formulated as alternatives to antibiotic treatment to upgrade animal health and productivity, and are essential for maintaining the balance of the gut microbiota. The treatment of calves with probiotic supplementation has emerged as a significant area of research. This review highlights the research progress on the pathogenesis of neonatal calf diarrhea and the mechanism of action of probiotics to provide new insights into the prevention and treatment of diarrhea in calves.

Mastitis, a common inflammatory condition in female mammals, increases the risk of breast cancer and causes substantial economic losses. Although antibiotics effectively treat mastitis, their overuse poses a threat to public health and safety. Pleurotus eryngii polysaccharides (PEPs) have emerged as a promising alternative to reduce antibiotic abuse; however, their protective mechanisms against mastitis remain unclear. This study aimed to elucidate the structural features of PEP and explore its protective effects against mastitis. Structural analysis revealed that PEP (Mw = 15.9 kDa) consists of galactose (60.66 %), mannose (37.51 %), glucose (1.11 %), and fucose (0.72 %), with a backbone composed of →2,6)-α-D-Galp-(1→ and →6)-α-D-Galp-(1→ residues, branched at C-2. In a lipopolysaccharide (LPS)-induced mouse mastitis model, PEP substantially reduced pro-inflammatory cytokine levels, enhanced antioxidant enzyme activity, alleviated mammary epithelial cell apoptosis, and restored blood-milk barrier integrity by modulating the nuclear factor-kappa B and Nrf2/HO-1 signaling pathways. Gut microbiota analysis showed PEP treatment increased the abundance and diversity of beneficial bacteria while reducing potentially harmful taxa. Metabolomic analysis results revealed the downregulation of metabolites such as riboflavin-5-phosphate and progesterone. Overall, PEP protects against mastitis by modulating the gut microbiota and metabolism, potentially via the gut-mammary axis, providing a theoretical basis for its clinical application.

Cryptosporidium spp. and G. duodenalis often infect humans, cats, and other mammals, causing diarrhea and being responsible for numerous outbreaks of waterborne and foodborne infections worldwide. The rapid increase in the number of pet cats poses a substantial public health risk. However, there were few reports about the infection of Cryptosporidium spp. and G. duodenalis infections in pet cats in Henan Province, central China. Thus, to understand the prevalence and genetic distribution of Cryptosporidium spp. and G. duodenalis in pet cats, and to evaluate the zoonotic potential, possible transmission routes and public health implications of isolates, fecal samples (n=898) were randomly collected from pet cats in 11 cities in Henan Province, central China. Nested PCR based on the SSU rRNA gene and bg gene was used to the prevalence of Cryptosporidium spp. and G. duodenalis, respectively. The prevalence was 0.8% (7/898) and 2.0% (18/898) for Cryptosporidium spp. and G. duodenalis respectively. Additionally, the Cryptosporidium spp. positive isolates were identified as C. parvum subtype IIdA19G1 by gp60 gene. In the present study, the IIdA19G1 subtype was discovered in pet cats for the first time in China, enriching the information on the host type and geographical distribution of Cryptosporidium spp. in China. For G. duodenalis, a total of 18 G. duodenalis positive samples were identified, belonging to four assemblages: a zoonotic assemblage A1 (4/898), three host-specific assemblages C (8/898), D (5/898), and F (1/898). Interestingly, we found that pet cats infected with Cryptosporidium spp. and G. duodenalis are more likely to experience emaciation symptoms compared to the negative group. More importantly, the prevalence of Cryptosporidium spp. and G. duodenalis detected in the present study were low, but the subtype IIdA19G1 of Cryptosporidium spp. and the assemblages A1, C, D, and F of G. duodenalis have the potential for zoonotic transmission. Thus, we should focus on preventing and controlling the risk of cross-species transmission that may occur in pet cats in Henan Province.

Mulberry leaf polysaccharides (MLP) are integral components of Mulberry leaves that confer hypoglycemic and hypolipidemic properties. This study investigated the efficacy of MLP in treating Type 2 Diabetes Mellitus (T2DM) and the underlying mechanisms related to gut microbiota-bile acids metabolism in T2DM rats. The findings revealed that MLP apparently reduced fasting blood glucose and lipid levels, ameliorated disorders in glucose and lipid metabolism, and mitigated insulin resistance. MLP enhanced the abundance of Prevotella, Ruminococcus, and Lactobacillus, thereby rectifying the gut microbiota dysbiosis in rats, which effectively restored gut microbiota homeostasis and composition. Furthermore, the data demonstrated that MLP modulated bile acid metabolism, as evidenced by reduced serum cholesterol levels, enhanced mRNA expression of hepatic cholesterol 7α- hydroxylase (Cyp7a1) and cholesterol 12α- hydroxylase (Cyp8b1), and ileal G protein-coupled bile acid receptor (Tgr5), while suppressing hepatic and ileal farnesoid X receptor (Fxr) mRNA expression in T2DM rats. Additionally, MLP upregulated the protein expression of hepatic CYP7A1 and CYP8B1, and ileal TGR5, while inhibiting FXR protein levels in the liver and ileum of T2DM rats. These results suggest that MLP can rectify disorders in glucose and lipid metabolism via the gut microbiota-bile acids metabolic pathway.

Background Enterocytozoon bieneusi is a zoonotic pathogen widely distributed in animals and humans. It can cause diarrhea and even death in immunocompromised hosts. Approximately 800 internal transcribed spacer ( ITS ) genotypes have been identified in E. bieneusi . Farmed foxes and raccoon dogs are closely associated to humans and might be the reservoir of E. bieneusi which is known to have zoonotic potential. However, there are only a few studies about E. bieneusi genotype identification and epidemiological survey in foxes and raccoon dogs in Henan and Hebei province. Thus, the present study investigated the infection rates and genotypes of E. bieneusi in farmed foxes and raccoon dogs in the Henan and Hebei provinces. Result A total of 704 and 884 fecal specimens were collected from foxes and raccoon dogs, respectively. Nested PCR was conducted based on ITS of ribosomal RNA ( rRNA ), and then multilocus sequence typing ( MLST ) was conducted to analyze the genotypes. The result showed that infection rates of E. bieneusi in foxes and raccoon dogs were 18.32% and 5.54%, respectively. Ten E. bieneusi genotypes with zoonotic potential ( NCF2 , NCF3 , D , EbpC , CHN-DC1 , SCF2 , CHN-F1 , Type IV , BEB4 , and BEB6 ) were identified in foxes and raccoon dogs. Totally 178 ITS -positive DNA specimens were identified from foxes and raccoon dogs and these specimens were then subjected to MLST analysis. In the MLST analysis, 12, 2, 7 and 8 genotypes were identified in at the mini-/ micro-satellite loci MS1 , MS3 , MS4 and MS7 , respectively. A total of 14 multilocus genotypes were generated using ClustalX 2.1 software. Overall, the present study evaluated the infection of E. bieneusi in foxes and raccoon dogs in the Henan and Hebei province, and investigated the zoonotic potential of the E. bieneusi in foxes and raccoon dogs. Conclusions These findings expand the geographic distribution information of E. bieneusi’ host in China and was helpful in preventing against the infection of E. bieneusi with zoonotic potential in foxes and raccoon dogs.

In this study, mammary epithelial cells (MAC-T) cells were used as models to investigate the effects of Lipopolysaccharides (LPS) on oxidative stress, inflammation, autophagy, and apoptosis, as well as the role of the AMPK/mTOR/ULK1 pathway in LPS-induced inflammatory damage. CCK-8 and lactate dehydrogenase (LDH) assays were used to detect MAC-T cell activity. Hoechst 33342 stained and evaluated the nuclear morphology of MAC-T cells. Real-time quantitative PCR and western blotting were used to detect the expression levels of genes and proteins related to autophagy, apoptosis, inflammation, and oxidative stress, respectively. The results showed that LPS inhibited the proliferation of MAC-T cells, upregulated the expression of inflammatory factors, increased oxidative stress levels, activated autophagy, and induced apoptosis. The AMPK/mTOR/ULK1 pathway was involved in the regulation of LPS-induced autophagy and apoptosis of MAC-T cells. Conclusion LPS regulates autophagy and apoptosis of MAC-T cells through the AMPK/mTOR/ULK1 pathway. Increased autophagy in MAC-T cells blocks the flow of autophagy, thereby promoting apoptosis.

Pentatrichomonas hominis ( P. hominis ) is a zoonotic parasite that affects a wide range of hosts, causing gastrointestinal diseases. The present study aimed to evaluate the prevalence of P. hominis among caged foxes and raccoon dogs and the effect of P. hominis on the gut microbiota in female foxes. A total of 893 fresh fecal samples were collected from the Hebei and Henan Provinces in China. P. hominis was screened based on 18S rRNA gene expression via nested PCR. The difference in the gut microbiota between nine P. hominis -positive and nine P. hominis -negative samples was investigated by 16S rRNA gene sequencing. The total prevalence of P. hominis infection in foxes and raccoon dogs was 31.7% (283/893). The prevalence rates of P. hominis infection were 28.2% (88/312) and 33.6% (195/581) in foxes and raccoon dogs, respectively. Phylogenetic analysis revealed that all P. hominis strains detected in foxes and raccoon dogs in the present study were the zoonotic genotype CC1. Moreover, compared with those in the P. hominis -negative group, the diversity of the gut microbiota in the P. hominis -positive group was lower, and the abundance of Firmicutes and the ratio of Firmicutes/Bacteroidetes (F/B) in the P. hominis -positive group were lower than those in the P. hominis -negative group. We speculate that these differences may be due to indigestion and diarrhea in infected female foxes. Overall, the present study evaluated the prevalence of P. hominis in foxes and raccoon dogs in the Henan and Hebei Provinces and revealed that P. hominis infection interrupted the diversity of the gut microbiota in female foxes.

Mulberry (Morus alba L.) leaf, as a medicinal and food homologous traditional Chinese medicine, has a clear therapeutic effect on type 2 diabetes mellitus (T2DM), yet its underlying mechanisms have not been totally clarified. The study aimed to explore the mechanism of mulberry leaf in the treatment of T2DM through tandem mass tag (TMT)—based quantitative proteomics analysis of skeletal muscle. The anti-diabetic activity of mulberry leaf extract (MLE) was evaluated by using streptozotocin-induced diabetic rats at a dose of 4.0 g crude drug /kg p.o. daily for 8 weeks. Fasting blood glucose, body weight, food and water intake were monitored at specific intervals, and oral glucose tolerance test and insulin tolerance test were conducted at the 7th and 8th week respectively. At the end of the experiment, levels of glycated hemoglobin A1c, insulin, free fat acid, leptin, adiponectin, total cholesterol, triglyceride, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol were assessed and the pathological changes of rat skeletal muscle were observed by HE staining. TMT-based quantitative proteomic analysis of skeletal muscle and bioinformatics analysis were performed and differentially expressed proteins (DEPs) were validated by western blot. The interactions between the components of MLE and DEPs were further assessed using molecular docking. After 8 weeks of MLE intervention, the clinical indications of T2DM such as body weight, food and water intake of rats were improved to a certain extent, while insulin sensitivity was increased and glycemic control was improved. Serum lipid profiles were significantly reduced, and the skeletal muscle fiber gap and atrophy were alleviated. Proteomic analysis of skeletal muscle showed that MLE treatment reversed 19 DEPs in T2DM rats, regulated cholesterol metabolism, fat digestion and absorption, vitamin digestion and absorption and ferroptosis signaling pathways. Key differential proteins Apolipoprotein A-1 (ApoA1) and ApoA4 were successfully validated by western blot and exhibited strong binding activity to the MLE’s ingredients. This study first provided skeletal muscle proteomic changes in T2DM rats before and after MLE treatment, which may help us understand the molecular mechanisms, and provide a foundation for developing potential therapeutic targets of anti-T2DM of MLE.

The incidence of liver-related complications in type 2 diabetes mellitus (T2DM) is rapidly increasing, which affects the physical and mental health of T2DM patients. Mulberry leaf flavonoids (MLF) were confirmed to have certain effects on lowering blood glucose and anti-inflammation. In this study, the high-fat diet (HFD) + STZ method was used to establish T2DM rat model and the MLF was administered by gavage for eight weeks. During the experiment, body weight and blood glucose level were measured at different time points. The pathological changes of rat liver were observed by H&E staining. The serum glucolipid metabolic indicators of serum, fasting insulin (FINS), and inflammatory factors levels were detected by ELISA. The expression levels of toll-like receptor 4 (TLR4), TNF receptor-associated factor 6 (TRAF6), myeloid differentiation factor 88 (MyD88), inhibitor of NF-κB alpha (IκΒα), p-IκΒα, and nuclear factor kappa-B (NF-κB)/p65 protein in liver tissue were measured by Western Blot. After 8 weeks' MLF treatment, the blood glucose of rats showed a downward trend; glycolipid metabolism level and insulin resistance were improved, which suggested that MLF could improve the disorder of glucose and lipid metabolism. The pathological damage and inflammation of the liver in T2DM rats were significantly improved, the levels of related serum inflammatory factors were reduced, and the expression of liver tissue-related proteins was downregulated. Our results indicated that MLF could reduce blood glucose and inhibit the development of liver inflammation. The mechanisms may be associated with the activation of TLR4/MyD88/NF-κB signal pathway to reduce the levels of inflammatory factors in serum.

目的 观察当归饮子口服联合亚甲蓝封闭治疗血虚风燥型肛周湿疹的临床疗效.方法 选择2019年1月—2020年8月北京中医药大学东方医院西院区肛肠科门诊收治的血虚风燥型肛周湿疹患者100例,按照随机数字表法分为观察组和对照组,各50例.观察组采用当归饮子内服联合亚甲蓝封闭治疗,对照组仅采用亚甲蓝封闭治疗,均以7 d为1个疗程,治疗2个疗程.观察2组治疗后总有效率,治疗前后肛周瘙痒、皮损面积、皮损形态评分,3个月内的复发率,不良反应.结果 观察组总有效率(96.0％)高于对照组(74.0％),差异有统计学意义(P＜0.05);治疗后观察组肛周瘙痒、皮损面积、皮损形态评分、复发率均低于对照组(P＜0.05);治疗期间2组均未发生严重不良反应.结论 当归饮子口服联合亚甲蓝封闭治疗血虚风燥型肛周湿疹疗效显著、复发率低、且安全性高.

Abstract Purpose To investigate the relationship between the susceptibility to type 2 diabetes and gut microbiota and explore the potential mechanisms. Methods Thirty-two SPF SD rats were raised as the donor rats, and divided into control, type 2 diabetes mellitus (T2DM) and Un-mod groups. Feces were collected and prepared as fecal bacteria supernatant A (T2DM group), B (Un-mod group) and Con (control group). Another seventy-nine SPF SD rats were separated into normal saline (NS) and ABX groups. ABX and NS groups were given antibiotics solution and normal saline, respectively. And then, the ABX group were randomly separated into the ABX1 (4-weeks ordinary diet), ABX2 (4-weeks HFD and STZ ip), FMT-A (fecal microbiota A transplantation, 4-weeks HFD and STZ ip), FMT-B (fecal microbiota B transplantation, 4-weeks HFD and STZ ip) and FMT-Con (normal fecal microbiota transplantation, 4-weeks HFD and STZ ip) groups. The NS group were randomly divided into the NS1 (4-weeks ordinary diet) and NS2 (4-weeks HFD and STZ ip) groups. The short-chain fatty acids (SCFAs) in feces were detected by gas chromatography using 16S rRNA gene sequencing. G protein-coupled receptor 41 (GPR41) and GPR43 were detected by Western blot and quantitative real-time polymerase chain reaction. Results g__Ruminococcus_gnavus_group were increased obviously in the FMT-A group (vs ABX2 or FMT-B group). Blood glucose levels, serum insulin, total cholesterol levels, triglyceride levels, and low-density lipoprotein cholesterol levels were evidently increased in the FMT-A group than ABX1 or ABX2 group. It was found that both the FMT-A and FMT-B groups had evidently higher contents of acetic acid and butyric acid (vs ABX2 group). In both FMT-A and FMT-B groups, GPR41 protein expression and GPR43 mRNA and protein expression increased. Conclusions G__Ruminococcus_gnavus_group may cause T2DM susceptibility, and T2DM susceptible flora transplantation can evidently increase the susceptibility to T2DM. It is possible that gut microbiota-SCFAs-GPR41/GPR43 play a role in the development of T2DM. A new treatment strategies and methods may be to develop pharmaceutical treatments that reduce blood glucose by controlling gut microbiota.

现代社会生活方式的改变,特别是高脂饮食和运动量减少使糖尿病发病率日益升高,已成为全球性的公共卫生问题,寻找有效的糖尿病治疗方法日益迫切.转化生长因子-β(TGF-β)信号通路与糖尿病并发症、肿瘤关系的研究较多,但其在糖尿病发生的作用尚未阐明.TGF-β信号通路可被多种因素激活,直接或间接导致胰岛β细胞凋亡和胰岛素抵抗(IR),有望成为糖尿病治疗的重要新靶点.TGF-β相关信号通路包括腺苷酸活化蛋白激酶(AMPK)、糖基化终产物受体、c-Myc、SnoN、Smurf1、miR-335-5P等信号分子,参与IR、胰岛β细胞凋亡、胰岛素分泌障碍、脂肪细胞纤维化表型及脂肪细胞代谢障碍的发生发展,并抑制白色脂肪棕色化,在人类糖尿病病理过程中发挥重要作用.中医认为糖尿病的病机为气阴两虚,后期除气虚外兼有阳虚血瘀,治以益气养阴,后期兼有温阳活血.研究发现部分中药和复方治疗糖尿病的作用与其对TGF-β信号通路的抑制高度相关.现综述TGF-β信号分子相关多条信号通路,阐明其在糖尿病形成过程中的病理机制,并就治疗糖尿病的中药复方与TGF-β信号通路相关性进行展望性分析.为治疗糖尿病的研究提供一定的理论依据.

坏疽性脓皮病(PG)是一种复杂的嗜中性粒细胞皮肤病[1-2],临床少见,且现代医学对于坏疽性脓皮病的发病机制尚不明确,临床治疗挑战巨大.代红雨教授专研难愈性创面,临床经验丰富,在运用中医中药治疗坏疽性脓皮病见解独到,疗效显著,现分享医案1例,并做简要分析如下.

The widespread fungal toxin Aflatoxin B1 (AFB1) is an inevitable pollutant affecting the health of humans, poultry, and livestock. Although studies indicate that AFB1 is hepatotoxic, there are few studies on AFB1-induced hepatotoxicity in sheep. Thus, this study examined how AFB1 affected sheep liver function 24 h after the animals received 1 mg/kg bw of AFB1 orally (dissolved in 20 mL, 4% v/v ethanol). The acute AFB1 poisoning caused histopathological injuries to the liver and increased total bilirubin (TBIL) and alkaline phosphatase (AKP) levels. AFB1 also markedly elevated the levels of the pro-inflammatory cytokines TNF-α and IL-6 while considerably reducing the expression of antioxidation-related genes (SOD-1 and SOD-2) and the anti-inflammatory gene IL-10 in the liver. Additionally, it caused apoptosis by dramatically altering the expression of genes associated with apoptosis including Bax, Caspase-3, and Bcl-2/Bax. Notably, AFB1 exposure altered the gut microbiota composition, mainly manifested by BF311 spp. and Alistipes spp. abundance, which are associated with liver injury. In conclusion, AFB1 can cause liver injury and liver dysfunction in sheep via oxidative stress, inflammation, apoptosis, and gut-microbiota disturbance.