This review summarizes the regulatory roles of polyphenolic compounds in animal skeletal health through the gut-bone axis and explores their benefits for animal nutrition. First, this review focuses on their key roles in maintaining skeletal homeostasis through gut microbiota, intestinal barrier integrity, immune regulation, microbial metabolites, and endocrine signaling. Then, from a biological mechanism perspective, we summarize how polyphenolic compounds regulate animal bone metabolism by reshaping gut microbiota composition, promoting short-chain fatty acid production, enhancing intestinal barrier function, reducing oxidative stress and systemic inflammation, and modulating osteogenic and osteoclastic signaling pathways. Furthermore, this review comprehensively discusses representative subclasses of polyphenolic compounds (including flavonoids, phenolic acids, lignans, stilbenes, and other bioactive compounds) and elucidates their mechanisms in animal skeletal protection and nutritional regulation. In conclusion, this review provides a theoretical foundation for understanding the polyphenol-mediated gut-bone axis regulatory mechanisms and offers new insights into nutritional strategies for promoting bone health in animals.

This study aimed to evaluate the therapeutic effects of platelet-rich plasma (PRP) and Cervus and Cucumis polypeptide (CCP) injections in rats with post-traumatic osteoarthritis (OA). The model was established by transection of the anterior cruciate ligament, and the animals were subsequently treated with PRP and CCP. Articular cartilage degeneration was assessed through gross morphological observation, histopathological staining, and a standardized scoring system. Concurrently, pain-related behaviors, joint swelling, levels of inflammatory cytokines, and markers associated with extracellular matrix degradation were measured. The results demonstrated that, compared with the OA model group, PRP and CCP exhibited varying degrees of functional improvement, specifically, a reduction in pain-related behaviors and an alleviation of joint swelling. Furthermore, cartilage morphological damage was diminished, inflammatory marker levels decreased, and indicators of extracellular matrix degradation were attenuated. Histopathological examination of liver and kidney tissues revealed no apparent abnormalities. This study provides valuable experimental evidence for further treatment strategies for OA.

Xylazole is a sedative and analgesic agent widely used in Chinese veterinary practice, valued for its convenient administration and effectiveness. This study aimed to clarify its mechanism of action by investigating the effects on cAMP and monoamine neurotransmitters using both in vitro and in vivo rat models. In rat cortical neurons, Xylazole increased cAMP levels in a concentration- and time-dependent manner, transiently increased extracellular DA levels, which subsequently declined, consistently reduced extracellular NE levels, and enhanced extracellular 5-HT along with its metabolite 5-HIAA. In contrast, in vivo administration in adult rats reduced cAMP, DA, and NE levels across multiple brain regions, including the cerebrum, hippocampus, and brainstem, while increasing 5-HT and 5-HIAA. Notably, in the cerebellum group, cAMP was elevated after drug washout, a pattern not observed in the other brain regions. These findings reveal a striking divergence: in P7 cortical neurons, Xylazole triggers an α2-adrenoceptor-dependent cAMP elevation, whereas in adult brain regions, a high concentration of locally delivered Xylazole leads to predominantly inhibitory cAMP changes, with a notable delayed increase in the cerebellum. Because of the non-physiological concentration used in reverse microdialysis, the in vivo neurochemical patterns should be regarded as exploratory regional responses, not as evidence of specific receptor-mediated mechanisms.

Recent evidence suggests a potential link between diabetes and the worsening and severity of osteoarthritis (OA) symptoms. Melatonin (MLT) has a strong ability to scavenge reactive oxygen species and lipid peroxidation, and plays a vital role in the treatment of OA. However, the role and mechanism of MLT in diabetic OA are still unclear. This study aimed to confirm that diabetes aggravates OA cartilage degeneration and to explore the specific mechanism by which MLT inhibits cell pyroptosis and alleviates OA. In this study, a model of OA combined with type 2 diabetes was established, and it was found that hyperglycemia would exacerbate the degradation of OA cartilage tissue. Secondly, we investigated the effect of MLT on OA under hyperglycemic conditions and the underlying molecular mechanisms in vivo and in vitro experiments. The results show that MLT inhibits the activation of the NLRP3 inflammasome in chondrocytes by activating PKG to mediate the Nrf2/HO-1 antioxidant defense system, thereby exerting anti-inflammatory, anti-pyroptosis, and anti-degradation effects on the cartilage extracellular matrix (ECM). Further verification revealed that silencing PKG or inhibiting Nrf2 would partially reduce the protective effect of MLT. MLT can also reduce the pain sensitivity of rats, decrease the degree of subchondral bone remodeling, and improve the microstructure of the bone. This suggests that MLT therapy may be a promising new approach for treating OA, particularly in patients with diabetes.

A 6.08 kg female stray Arctic fox (Vulpes lagopus) of unknown age was presented with tail gland inflammation. Initial conventional therapy and subsequent tail amputation at a primary veterinary facility resulted in limited improvement. Subsequently, a topical medication red mercuric oxide (Hydrargyri Oxydum Rubrum) was applied for 4 weeks. Although the local infection showed signs of improvement, the fox subsequently developed progressive systemic signs, including anorexia, dark urine, and weight loss, prompting referral. Clinical examination revealed a large amount of cherry-red medication covering the wound. Hematological tests indicated elevated neutrophils and C-reactive protein (CRP), suggesting an inflammatory response. Serum biochemistry revealed elevated levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bile acids (TBA), indicating hepatobiliary injury, alongside an elevated creatine kinase (CK) suggestive of abnormal muscle metabolism. The whole-blood mercury concentration was significantly elevated (4.7583 μg/L). Imaging findings included: ultrasound showing gallbladder sludge, abnormal liver parenchyma echogenicity, and indistinct kidney contours; X-ray revealed gastric gas, liver edge extending beyond the costal arch, blurred renal contours, and significantly increased density in the tail gland area. The Arctic fox was diagnosed with chronic topical mercury (II) oxide-induced mercury poisoning and secondary liver injury. The treatment regimen included: (1) removal of the topical medication and surgical debridement; (2) intravenous administration of reduced glutathione (hepatoprotection), ceftiofur sodium (anti-infective), and vitamin C (antioxidant); (3) oral administration of a mercury chelating agent (dimercaptosuccinic acid) and choleretics (ursodeoxycholic acid); and (4) intramuscular injection of appetite stimulants. After 4 weeks of systemic treatment, the fox’s abnormal biochemical parameters returned to normal, and the prognosis was good. This case addresses a specific gap in the diagnosis and treatment of heavy metal poisoning in wildlife. It provides a valuable reference for the clinical management of poisoning cases associated with topical mercury-containing wound medications.

This study explored the potential mechanism of SIRT1 in bovine osteoarthritis (OA). In vivo experiments evaluated the severity of damage to bovine tarsal cartilage tissue through pathological staining and Mankin scoring. When compared with healthy bovines, cartilage in OA-affected bovines displayed ECM degradation and increased Mankin scores (P<0.01). In the cartilage of OA-affected cattle, the protein expression of inflammatory factors (TNF-alpha, IL-1(3, COX-2) and ECM degradation markers (MMP-3, MMP-13) was increased (P<0.05), the expression levels of key pathway proteins (including SIRT1, nuclear Nrf2 and HO-1) were decreased (P<0.05), and the expression of nuclear p65 and p-I kappa B alpha was upregulated (P<0.05). In vitro studies, we developed a bovine primary chondrocyte inflammation model using 10ng/mL IL-1(3. IL-1(3 treatment significantly upregulated the expression levels of ECM degradation markers in chondrocytes (P<0.01). Transmission electron microscopy revealed mitochondrial ultrastructural damage, and flow cytometry indicated an apoptosis rate of 38.1%. ML334 treatment significantly enhanced the levels of nuclear Nrf2, HO-1, and Bcl-2 (P<0.05), while simultaneously decreasing nuclear p65, BAX, Cleaved caspase-3, and ECM degradation markers (P<0.05). JSH-23 treatment successfully downregulated nuclear p65 and ECM degradation marker levels (P<0.05). Treatment with the SIRT1 agonist SRT2104 not only increased the level of SIRT1, nuclear Nrf2, and HO-1 (P<0.05), but also effectively attenuated the expression of nuclear p65 (P<0.05). This experiment strongly supports the claim that SIRT1 effectively protects bovine cartilage ECM from degradation and apoptosis through a dual mechanism of action (activation of the Nrf2/HO-1 pathway and inhibition of the NF-kappa B pathway).

As one of the most consumed meat products globally, microplastics (MPs) residues in chickens may enter the human body through the food chain. Therefore, this study aimed to investigate the adverse effects of MPs exposure on chicken health and the detoxification mechanisms of astaxanthin (AST). We found that MPs significantly impaired liver function, inducing injury characterized by hepatocyte ferroptosis, inflammation, lipid disorder, and fibrosis. This hepatic damage was linked to MPs-induced gut microbiota dysbiosis and disruption of the intestinal barrier. AST exerted hepatoprotective effects by activating the Nrf2/HO-1 signaling pathway and attenuating hepatic oxidative stress and ferroptosis. In parallel, AST improved gut microbiota composition and intestinal barrier integrity, thereby potentially reducing gut-derived inflammatory burden. Together, these findings suggest that AST confers liver protection through both direct hepatic actions and indirect modulation of the gut-liver axis.

Musculoskeletal injuries represent a primary cause of suboptimal performance and early retirement in equine athletes. To address this challenge, the veterinary community has long endeavored to develop safer and more effective therapeutic strategies. Extracorporeal shock wave therapy (ESWT), as a treatment for equine musculoskeletal injuries, has garnered substantial attention among equine veterinarians. Focused on the theme ESWT Therapy for Equine Musculoskeletal Disorders: From biological mechanisms to clinical applications, this article systematically reviews existing literature on the biological effects of ESWT—including analgesia, anti-inflammation, and autologous repair—mediated through diverse signaling pathways and factors. It synthesizes the current status of clinical applications and underlying mechanisms of ESWT in managing equine musculoskeletal conditions such as suspensory desmitis, superficial digital flexor tendinitis, osteoarthritis, navicular syndrome, and back pain syndrome. Additionally, the article summarizes relevant parameters for ESWT in treating different injuries, offering a reference for clinical equine veterinarians.

INTRODUCTION:This review summarizes the application of nanomaterial-mediated intra-articular targeted drug delivery systems in the treatment of osteoarthritis (OA) and their regulatory mechanisms on key cellular signaling pathways. Studies have shown that novel nanocarriers can effectively load, deliver, and controllably release therapeutic agents, significantly enhancing drug bioavailability and reducing systemic toxicity. By precisely modulating signaling pathways, nanomaterials (NM) can effectively suppress inflammatory responses, alleviate oxidative stress, promote chondrocyte anabolism, delay extracellular matrix degradation, and regulate programmed cell death. This study highlights the potential of NM as a multi-target, synergistic therapeutic strategy for OA intervention, providing a theoretical and experimental basis for the development of next-generation precision therapies for OA. AREAS COVERED:This paper reviews the research progress of nano-drug delivery technology in the treatment of joint diseases, focusing on the potential mechanisms of targeted drug delivery and retention, promoting regeneration and repair, and realizing anti-inflammatory and antioxidant effects. We identified relevant literature through PubMed and Web of Science, focusing on studies published over the past five years. EXPERT OPINION:Nanomaterials for osteoarthritis treatment are evolving from passive drug carriers to intelligently responsive, targeted multifunctional systems capable of personalized, proactive, and regenerative therapy, overcoming current limitations in toxicity and delivery precision.

Ketamine, an N-methyl-D-aspartate receptor antagonist with anesthetic and analgesic properties, is extensively utilized for the induction and maintenance of pediatric perioperative anesthesia. Increasing evidence suggests that prolonged exposure to ketamine may induce neurotoxicity in developing animals, adversely affecting their long-term cognitive function. N-acetylcysteine (NAC) is an organic sulfur compound in the Allium genus; however, the mechanisms through which it alleviates ketamine-induced neurotoxicity during developmental stages remain inadequately understood. Refine the investigation of the mechanisms by which Nac mitigates ketamine-induced neurotoxicity during development via ferroptosis and pyroptosis pathways. Postnatal day 7 in SD rats PC12 cells and HAPI cells were used in this study. The neuroprotective mechanism of Nac was elucidated through pathological, histological, and molecular biological methodologies to assess pyroptosis, ferroptosis, hippocampal tissue damage, and behavioral modifications in adulthood. The results suggest that prior administration of Nac reduced lipid peroxidation and mitochondrial injury, along with pyroptosis activated by the NLRP3/caspase-1 pathway, hippocampal damage, and cognitive deficits after exposure to ketamine. In summary, our findings from both in vivo and in vitro studies indicate that ROS plays a significant regulatory role in the neurotoxic effects of ketamine during development. Furthermore, Nac mitigates hippocampal damage and cognitive deficits associated with ketamine exposure by inhibiting ROS-mediated ferroptosis and pyroptosis.

Cefquinome is used to treat septicemia caused by Escherichia coli (E. coli) and respiratory infections caused by Streptococcus equi subsp. zooepidemicus in foals. However, studies reporting the use of cefquinome to target E. coli as pathogens of sepsis are lacking. Therefore, this study aimed to determine the optimal dosage regimen for cefquinome against E. coli using a PK/PD model. After the administration of 1 mg/kg cefquinome (intramuscularly or intravenously), blood samples were collected at different time points to determine the serum concentration of cefquinome via HPLC. The pharmacokinetic parameters were evaluated via NCA (WinNonlin 5.2.1 software). The main pharmacokinetic parameters of cefquinome in foals were as follows: after intravenous administration, the elimination half-life (T1/2β) was 2.35 h, the area under the curve (AUC0–last) was 12.33 μg·h/mL, the mean residence time (MRT0–last) was 2.67 h, and the clearance rate (CL) was 0.09 L/h/kg. After intramuscular administration, the peak concentration (Cmax) was 0.89 μg/mL, the time to reach the maximum serum concentration (Tmax) was 2.16 h, T1/2β was 4.16 h, AUC0–last was 5.41 μg·h/mL, MRT0–last was 4.92 h, CL was 0.15 L/h/kg, and the absolute bioavailability (F) was 43.86%. An inhibitory sigmoid Emax model was used to integrate the PK/PD indices with ex vivo antimicrobial effects to identify pharmacodynamic targets (PDTs). According to the dose calculation formula, the doses of intramuscularly administered cefquinome required to achieve bacteriostatic effects, bactericidal effects, and bactericidal elimination were 1.10, 1.66, and 2.28 mg/kg, respectively. However, further studies are warranted to verify the therapeutic efficacy of cefquinome in clinical settings.

Autophagy and pyroptosis in chondrocytes contribute to cartilage degeneration in osteoarthritis (OA). Capsaicin (Cap), a bioactive compound derived from chili peppers, exhibits anti-inflammatory and antioxidant properties. However, the underlying mechanisms by which Cap exerts its chondroprotective effects in OA remain poorly understood. This study aims to elucidate the molecular basis of Capmediated chondroprotection. OA models were established using SD rats and primary rat chondrocytes to evaluate the effects of Cap on extracellular matrix (ECM) degradation, inflammation, pyroptosis, autophagy, and the AMPK/mTOR signaling pathway. To investigate the mechanisms underlying Cap's chondroprotective effects, 3-Methyladenine and dorsomorphin were employed to inhibit autophagy and AMPK signaling, respectively. Cap mitigates cartilage damage and alleviates pain through activation of the AMPK/mTOR signaling pathway, while promoting chondrocyte autophagy and suppressing NLRP3 inflammasome activation and subsequent inflammatory responses. Notably, inhibition of autophagy or AMPK signaling in chondrocytes partially abrogates the protective effects of Cap on cartilage. Our findings demonstrate that Cap exerts its therapeutic effects in OA by activating the AMPK/mTOR pathway and enhancing autophagy in chondrocytes, thereby sequentially inhibiting pyroptosis and ECM degradation.

Osteoarthritis is often exacerbated by obesity and metabolic syndrome, which are frequently associated with high-fat diets (HFD). This study investigates the direct effects of HFD on articular cartilage following anterior cruciate ligament transection (ACLT) in rats, while also examining the role of free fatty acids (FFA) on chondrocyte activity. Our findings indicate that short-term HFD treatment after ACLT reduces pain sensitivity, alleviates knee swelling, and mitigates cartilage damage. Joint imaging studies, along with serum analyses of inflammatory markers and extracellular matrix (ECM) degradation, further underscore the protective role of post-surgical HFD in maintaining cartilage integrity. Notably, HFD significantly enhances AMP-activated protein kinase (AMPK) phosphorylation in cartilage. In vitro experiments reveal that low concentrations of FFAs stimulate chondrocyte proliferation and energy metabolism, whereas AMPK inhibition leads to elevated expression of inflammatory mediators and ECM-degrading enzymes in chondrocytes. Collectively, these results suggest that short-term HFD following ACLT surgery exerts protective effects on cartilage, primarily through AMPK activation.

Ethnopharmacological relevanceGinkgo biloba, as the most widely available medicinal plant worldwide, has been frequently utilized for treat cardiovascular, cerebrovascular, diabetic and other diseases. Due to its distinct pharmacological effects, it has been broadly applications in pharmaceuticals, health products, dietary supplements, and so on. Ginkgolide C (GC), a prominent extract of Ginkgo biloba, possesses potential in anti-inflammatory and anti-oxidant efficacy.Aims of the studyTo determine whether GC mitigated the progressive degeneration of articular cartilage in a Monosodium Iodoacetate (MIA)-induced osteoarthritis (OA) rat model by inhibiting the activation of the NLRP3 inflammasome, and the specific underlying mechanisms.Materials and methodsIn vivo, an OA rat model was established by intra-articular injection of MIA. The protective effect of GC (10 mg/kg) on articular cartilage was evaluated. Application of ATDC5 cells to elucidate the mechanism of the protective effect of GC on articular cartilage. Specifically, the expression levels of molecules associated with cartilage ECM degrading enzymes, OS, ERS, and NLRP3 inflammasome activation were analyzed.ResultsIn vivo, GC ameliorated MIA-induced OA rat joint pain, and exhibited remarkable anti-inflammatory and anti- ECM degradation effects via inhibition of the activation of NLRP3 inflammasome, the release of inflammatory factors, and the expression of matrix-degrading enzymes in cartilage. Mechanically, GC inhibited the activation of NLRP3 inflammasome by restraining ROS-mediated p-IRE1α and activating Nrf2/NQO1 signal path, thereby alleviating OA. The ROS scavenger NAC was as effective as GC in reducing ROS production and inhibiting the activation of NLRP3 inflammasome.ConclusionsGC have exerted chondroprotective effects by inhibiting the activation of NLRP3 inflammasome.

Canine prostate is susceptible to diseases such as cysts, abscesses, and tumors. A 15-year-old male castrated Chinese rural dog underwent staged treatment. Preliminary diagnosis is based on examination results, including clinical symptoms (tenesmus, dysuria, frequent urination, and hematuria); hematology (elevated neutrophil count); X-rays (swelling of the prostate); ultrasound examination (less uniform echo in the prostate region, no echo effect in parenchyma); biopsy smear of prostate tissue (large number of neutrophils and rod-shaped bacteria). Therefore, the dog was preliminarily diagnosed with a prostate abscess. Antibiotic therapy was used for treatment. Three days later, the symptoms of hematuria and frequent urination did not improve, and the state was poor. The owner was advised to undergo surgical treatment-omental packing. Meanwhile, bacterial culture identification, drug sensitivity test and histopathological examination were performed. Pathological diagnosis was prostate adenocarcinoma. Subsequently, antibiotic therapy with enrofloxacin and antineoplastic maintenance therapy with mitoxantrone were administered. Six months later, the dogs were followed up, and the results showed no disease in the prostate tissue and no metastatic lesions. This is the report describing the use of omental packing for the treatment of prostate adenocarcinoma in dogs. In order to provide an important theoretical basis for the treatment of prostate cancer - omental packing into veterinary routine.

Fluoride is one of the essential trace elements for body. However, excessive fluoride poses a major threat to human and animal health. Fluorosis may cause pathological damage of the duodenum, but the underlying mechanism needs to be further studied. This study was to investigate the effects of long-term exposure to sodium fluoride (0, 500, 1,000, 2,000 mg/kg) on the duodenum of chickens. The results showed that after NaF exposure, intestinal epithelial cells were disarranged, necrotic or even exfoliated, goblet cells and mucus secretion were increased, and inflammatory response was induced in duodenal tissue. Oxidative stress, endoplasmic reticulum stress (ERs), and heat shock proteins (HSPs) are an adaptive response, however long-term, excessive changes are detrimental. Fluorosis activates ERs through IRE1, PERK and ATF6 pathways, increases the expression of HSP60, HSP70 and HSP90, and causes apoptosis and oxidative damage in duodenal tissue. In addition, fluorosis can activate the MAPK signaling pathway. This article can provide a reference for exploring the potential duodenal toxicity of sodium fluoride.

近3年来,受新冠疫情影响,国内农林院校动物医学专业学生的毕业实践实习工作面临着前所未有的教学困难.首先,疫情期间,学生不能出校,理论教学尚可通过线上进行系统性讲授,但校外毕业实践实习地点因疫情影响封闭不能正常营业接诊,使得连续的实践实习教学不能正常开展.其次,受疫情影响,大部分动物医院、科研机构等出现关闭状态,使本专业应参加实践实习的学生未能如期进行线下学习,导致学生在专业技能上与往届学生比较有所欠缺.第三,由于学生接触实践实习及社会的时间减少,导致目前毕业实践实习的学生主观惰性心理增强、对未来的盲目性和专业技能掌握能力下降,也是当前动物医学专业毕业前景不明确,就业困难,专业技能不完善的主要因素.针对以上疫情下动物医学专业学生的实际情况,东北农业大学动物临床教学医院制定了科学合理的应对策略措施.在保障基本实践实习教学的基础上,协助学生渡过这段艰难的时期.通过线上线下教学相结合,设立新课程及新教学模式应用,教学医院与校外企业相结合等多项措施,为动物医学专业学生毕业临床实践教学在疫情下的新教学模式的构建与实行打下基础.

Osteoarthritis (OA) is a chronic degenerative bone and joint disease that often occurs in aging animals. Currently, there are still no biomarkers that can effectively diagnose OA in the early stage. To identify possible biomarkers, here we examined changes in the expression of C‐telopeptide fragments of type II collagen (CTX‐II) and collagenase generated carboxy‐terminal neoepitope of type II collagen (C2C) in serum at different time points in an anterior cruciate ligament transection (ACLT)‐induced rat OA model. The serum levels of CTX‐II and C2C, and the OARSI score in the ACLT group were increased from week two until the end of the experiment. The AUC of the combined biomarkers was higher than that of CTX‐II or C2C alone. Moreover, serum levels of CTX‐II and C2C were positively correlated with the OARSI score. The results suggest that the combined detection of serum CTX‐II and C2C concentrations may have potential for assessing and diagnosing OA at early stages.

Cadmium (Cd), as one of the seventh most toxic heavy metal pollutants, widely persisted in the environment, leading to osteoblast dysfunction and ultimately Cd-related skeletal disease. However, the damaging effects of Cd on cellular functions and the potential pathogenic mechanisms are still unclear. In our study, Cd is believed to induce mitochondrial dysfunction and endoplasmic reticulum stress (ERS) in a dose-dependent manner, thereby leading to apoptosis, as evident by elevated Drp1, Fis1, GRP78, CHOP, ATF4, P-EIF2α, P-PERK, BAX, cleaved caspase 3 proteins expression and ROS levels, and decreased the levels of Mfn2, OPA1, Bcl2, and intracellular Collagen I, B-ALP, RUNX2, and BGP genes. Additionally, when the exogenous addition of NAC and 4-PBA was added, it was found that NAC and 4-PBA had a positive moderating effect on Cd-induced cell dysfunction. Mechanistically, Cd-induced oxidative stress and apoptosis by upregulating the PERK-EIF2α-ATF4-CHOP signaling pathway and inhibiting the Nrf2/NQO1 pathway. In conclusion, we found that Cd was involved in mitochondrial dysfunction, ERS, and apoptosis in MC3T3-E1 cells, While NAC and 4-PBA relieved ERS and attenuated cell apoptosis.