Renal failure is a common chronic disease in dogs that substantially affects both their quality of life and longevity. The objective of this study was to assess the protective mechanisms of baicalin in cisplatin-induced Madin–Darby canine kidney (MDCK) epithelial cells’ apoptosis model and explore the impacts of baicalin at varying doses on various indexes, such as cisplatin-induced MDCK cell apoptosis, oxidation and antioxidation, and inflammatory factors. (Methods) MDCK cells in the logarithmic growth phase were randomly divided into a control group, a model group (20 μmol/L cisplatin), and a baicalin-protection group (20 μmol/L cisplatin + 50, 25 μmol/L baicalin) and received the corresponding treatments for 24 h. The effects of cisplatin on MDCK cell apoptosis, oxidation and antioxidation, inflammatory factors, and other indicators were studied, and the relieving effect of baicalin on cisplatin-induced MDCK cell damage was explored. Calcein/PI staining and Annexin V-FITC/PI staining showed that cisplatin induced the apoptosis of MDCK cells, while baicalin effectively reduced the damage caused by cisplatin. The ELISA results demonstrated a significant elevation in the nitric oxide (NO) and malondialdehyde (MDA) levels within the MDCK cells following treatment with cisplatin (p < 0.01). In addition, superoxide dismutase (SOD), glutathione peroxidase (GSH), and catalase (CAT) activities remarkably declined (p < 0.01), while tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) expression within the MDCK cells were apparently elevated (p < 0.01). However, baicalin treatment resulted in opposite changes in these factors. The findings suggested that baicalin exhibits potential in mitigating cisplatin-induced oxidative stress and inflammation in MDCK cells. As revealed with the Western blot results, cisplatin promoted P62, P53, and BAX protein levels, increased mTOR phosphorylation, inhibited AMPK phosphorylation, and reduced Beclin1 and BCL-2 protein levels. However, a contrasting trend was observed following baicalin treatment. Cisplatin can inhibit the activity of MDCK cells, lead to abnormalities in oxidation and antioxidation functions and cell inflammatory factors, and accelerate cell apoptosis. Moreover, baicalin can significantly alleviate the damage of cisplatin to MDCK cells.

Platycladus orientalis leaves are rich in flavonoids and polysaccharides, which offer high medicinal and nutritional benefits. This study aimed to investigate the impact of P. orientalis leaf extract (PLE) on the growth performance, fur quality, serum parameters, and intestinal microbiota of raccoon dogs. Sixty healthy male black raccoon dogs, aged 85 (±5) days, were randomly assigned to four groups and fed a basal diet supplemented with 0, 0.25, 0.50, and 1.00 g/kg PLE for 125 days (designated as groups P0, P1, P2, and P3, respectively). The results revealed that the raccoon dogs in group P1 exhibited increased average daily gain and underfur length while showing a decreased feed/gain ratio compared to group P0 (p < 0.05). However, the heart index in group P2 was significantly lower than in group P0 (p < 0.05), and the kidney index and serum alanine aminotransferase activities in group P3 were higher than in groups P2 and P0 (p < 0.05), suggesting potential adverse effects at higher PLE dosages. Notably, dietary PLE supplementation led to a reduction in serum glucose concentrations (p < 0.05), which may have implications for glucose regulation. Furthermore, the study explored the impact of dietary supplementation with 0.25 g/kg PLE on the raccoon dogs’ intestinal microbiota using high-throughput sequencing. The results showed significant alterations in the microbial community structure, with a notable decrease in the abundance of Prevotella copri in response to 0.25 g/kg PLE supplementation (p < 0.05). In conclusion, supplementing raccoon dogs’ diet with 0.25 g/kg PLE can lead to improved growth performance and a positive influence on the intestinal microbiota. However, caution should be exercised regarding higher dosages, as they may have adverse effects on certain parameters. As a result, PLE holds promise as a potential feed additive for fur animal production.

The raccoon dog (Nyctereutes procyonoides) is a typical omnivore possessing wide dietary adaptability and tolerance to rough feeding, which may be attributed to its intestinal microbiota. The study aimed to investigate the effect of dietary alfalfa meal levels on the growth performance, nutrient apparent digestibility, serum parameters, and intestinal microbiota of raccoon dogs. Sixty raccoon dogs were randomly divided into four dietary treatments containing 0% (AM0), 5% (AM5), 10% (AM10), and 15% (AM15) alfalfa meal for a 60-day experiment. The results showed that compared to raccoon dogs fed the AM0 diet, those fed the AM5 and AM10 diets had no significant difference in growth performance, while those fed the AM15 diet experienced a significant decrease. Raccoon dogs fed the AM5 diet had no significant effect on the nutrient apparent digestibility. Dietary supplementation with alfalfa meal significantly decreased serum urea levels and increased the antioxidant capacity of raccoon dogs. The intestinal microbiome analysis showed that the richness and diversity of colonic microbiota significantly increased in the AM15 group. With the increase in dietary alfalfa meal levels, the relative abundance of fiber-degrading bacteria in the colon of raccoon dogs, such as Treponema, Phascolarctobacterium, and Christensenellaceae R-7 group, increased. However, the relative abundance of pathogenic bacteria, including Anaerobiospirillum, decreased. In conclusion, the inclusion of 5% alfalfa meal in the raccoon dogs’ diet had no effect on growth performance, but it exhibited the potential to improve serum antioxidant capacity and intestinal microbiota. This indicates that raccoon dogs have a certain tolerance to the addition of alfalfa meal in their diet.

The conservation of Siberian tigers, the apex predators in the Asia–Pacific region, hinges on a thorough understanding of their physiological statuses and adaptive mechanisms. In order to fill a critical gap in our knowledge of this endangered species, we conducted comprehensive analyses of Siberian tiger whole blood and serum using modern hematology and biochemical analyzers. The blood samples were collected from subadult (2–3 years old) Siberian tigers (n = 15 for hematological analysis and n = 7 for biochemical analysis). In the present study, distinct hematological patterns including an elevated mean platelet volume (MPV) and a higher red cell distribution width coefficient of variation (RDW-CV) were observed, which were possibly triggered by pre-anesthesia resistance movements. Notably, the neutrophil percentage in Siberian tigers was found to be significantly higher than that in domestic cats and Bengal tigers, suggesting species-specific immune adaptations. In addition, serum biochemical analysis provided refined parameter ranges for subadult tigers. Unlike previous studies encompassing a broader age range, our data specifically characterize biochemical profiles in subadult tigers, offering vital baselines for health monitoring and conservation strategies. These results not only enhance our understanding of the biology of Siberian tigers but also provide scientific support for targeted conservation efforts, fostering population recovery and ecological balance in their natural habitats.

Aflatoxin B₁ (AFB₁) is a common contaminant in canine diets that can cause significant damage to metabolic organs with prolonged exposure. Dihydromyricetin (DMY), a flavonoid compound abundant in Ampelopsis grossedentata, is widely used in functional foods due to its diverse biological activities. This study aimed to investigate the mechanism by which DMY alleviates AFB1-induced damage in MDCK cells. Four experimental groups were established: a control group with culture medium only (CON group), a group treated with 5 μg/mL AFB1 (AFB1 group), and two treatment groups treated with 5 μg/mL AFB1 combined with either 25 mmol/L or 50 mmol/L DMY—concentrations with more robust and stable protective effects than 100 mmol/L DMY, as confirmed by experimental screening. The results showed that AFB₁ significantly reduced MDCK cell viability at concentrations of 5–30 μg/mL (p < 0.01), while DMY at 25–100 mmol/L markedly improved cell viability (p < 0.01). AFB₁ treatment led to a significant increase in reactive oxygen species (ROS), malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) levels, along with a reduction in superoxide dismutase (SOD) and catalase (CAT) activities (p < 0.01). 25 mmol/L and 50 mmol/L DMY treatment reversed these effects, decreasing ROS, MDA, TNF-α, IL-6, and IL-1β levels while increasing SOD and CAT activities (p < 0.01). Furthermore, 25 mmol/L and 50 mmol/L DMY improved mitochondrial membrane potential (p < 0.01), counteracting AFB₁’s inhibitory effects on autophagy-related proteins by promoting p-AMPK and Beclin-1 expression while inhibiting p-mTOR, p53, and p62 expression (p < 0.05). In conclusion, DMY mitigates AFB₁-induced damage in MDCK cells by enhancing anti-inflammatory and antioxidant defenses and promoting autophagy, providing a theoretical foundation for future treatment strategies for canine kidney damage.