Metabolism-disorder-induced liver diseases have become increasingly prevalent worldwide and are clinically linked to obesity and type 2 diabetes. In addition, a large number of previous literature studies have indicated that plasma miR-130b is a promising biomarker for the early diagnosis and treatment of obesity. However, whether miRNA-130b that was positively correlated with obesity resulted in hepatic inflammation needs to be further studied. Therefore, the study aims to determine the effect of microvesicle-shuttled miRNA-130b (miR-130b-MV) on the hepatic inflammation and its potential mechanism in high-fat diet-induced obese mice. Three-week-old C57BL/6 mice were fed a high-fat diet for eight weeks. Then, the obese mice received tail vein injections of MV-packaged scrambled control microRNA (miR-SC-MV) or miR-130b-MV every other day for 10 days. Compared with the control group, the miR-130b-MV injection significantly reduced the body weight while increasing the ratio of liver wet weight to total body weight. In addition, the miR-130b-MV injection significantly activated the hepatic inflammation by increasing the expression of proinflammatory genes, although the plasma concentrations of IL-6 and TNF-α were only slightly increased. Furthermore, the miR-130b-MV injection significantly increased the hepatic miR-130b expression while significantly suppressing the protein expression and phosphorylation of GR, a potential target of miR-130b. Moreover, the miR-130b overexpression results in a decrease in the expression of endogenous GR protein and a decrease in the activity of the luciferase reporter of GR 3′-UTR. In addition, the miR-130b-MV injection significantly upregulated NF-kB (p50) in both the cytoplasm and nucleus, showing enhanced proinflammation response. The above results demonstrated that miR-130b-MV activated the hepatic inflammation by inhibiting GR-mediated immunosuppression in high-fat diet-induced obese mice, suggesting a novel mechanism underlying the obesity-induced hepatic inflammation, and the inhibition of miR-130b may serve as a new molecular therapeutic target for the prevention and treatment of hepatic inflammation.

Our previous studies have shown that miR-130b can significantly inhibit subcutaneous fat deposition in pigs. This study aims to further investigate its effect on lipid accumulation at early-stage (24 and 48 h) and late-stage (7 d) adipogenic differentiation and to clarify potential mechanisms using primary rat intramuscular preadipocytes (IMAs). Results showed that at 24 h and 48 h, miR-130b overexpression significantly reduced lipid deposition by inhibiting proliferation and inducing apoptosis. Furthermore, miR-130b overexpression significantly inhibited the expression of cell cycle and apoptosis marker genes. Specifically, the mRNA expression of Ccnd1 tended to decrease, while the BCL2 protein level was significantly decreased at 48 h. In contrast, miR-130b inhibition significantly increased the BCL2 protein level. At 7 d, the miR-130b mimic significantly decreased intracellular TG content and tended to decrease Hsd11b1 mRNA expression while significantly promoting Lpl mRNA expression. Additionally, the miR-130b mimic significantly increased the CASP3 protein level and tended to decrease the BCL2 protein level. In conclusion, our data indicated for the first time that miR-130b could reduce lipid deposition in rat IMAs through different mechanisms: at the early stage of differentiation by inhibiting proliferation and promoting apoptosis and at the late stage by inhibiting adipogenic differentiation, promoting lipid hydrolysis, and promoting apoptosis.

Rheumatoid arthritis (RA) is a chronic autoimmune disease that has a serious impact on both human health and animal production. The gut microbiota is a large and complex symbiotic ecosystem in animals, and the imbalance of gut microbiota is closely related to the pathogenesis of numerous diseases, including RA. The interactions among the gut microbiota, intestinal barrier, and immune system play key roles in maintaining intestinal homeostasis and affecting the development of RA. Regulating intestinal flora and metabolites provides new ideas for the prevention and treatment of RA. Probiotics can regulate the balance of intestinal flora and metabolites, improve the immune environment, and provide novel therapeutic strategies against RA. In order to summarize the role of gut microbiota and metabolite remodeling in the development and management of RA, this review will elaborate on the role of intestinal flora imbalance in the pathogenesis of RA and assess prospective therapeutic approaches that target the gut flora. Understanding the interaction among intestinal flora, metabolites, and RA will help to clarify the pathogenesis of RA and develop innovative and personalized therapeutic interventions against chronic autoimmune diseases.

Colitis is a chronic relapsing inflammatory disorder characterized by persistent mucosal inflammation, epithelial barrier disruption, oxidative stress, immune dysregulation, and gut microbiota imbalance. Although current therapies have improved disease management, their long-term use is still limited by incomplete response, relapse, adverse effects, and high cost. Natural products have attracted increasing attention as promising candidates for colitis intervention because of their structural diversity, broad bioactivity, and multitarget regulatory potential. In veterinary medicine, colitis and colitis-related intestinal inflammatory disorders are also clinically relevant in companion animals, horses, and food-producing animals, where they contribute to diarrhea, impaired intestinal barrier function, reduced performance, treatment costs, and antimicrobial-use concerns. Therefore, natural products may have additional value as adjunctive, nutritional, or microbiota-modulating strategies in veterinary and comparative gastroenterology. This review summarizes the major categories of natural products investigated for colitis, including flavonoids, polyphenols, alkaloids, terpenoids, saponins, polysaccharides, plant extracts, and traditional herbal formulas, and discusses their principal mechanisms of action, such as anti-inflammatory activity, attenuation of oxidative stress, restoration of intestinal barrier integrity, modulation of immune responses, regulation of gut microbiota, and control of programmed cell death. We also highlight the major limitations of current research, including overreliance on preclinical models, insufficient target validation, poor bioavailability, and limited clinical evidence. Overall, natural products represent an important source of therapeutic candidates for colitis, but their clinical translation will require deeper mechanistic studies, standardized evaluation, and well-designed clinical investigations. Importantly, future studies should distinguish phenotype-associated changes from causal mechanisms by integrating direct target engagement, functional rescue experiments, microbiota-causality validation, and standardized pharmacokinetic and safety assessment.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is one of the most prevalent chronic liver diseases worldwide, involving multiple pathological mechanisms such as lipid metabolism disorders, oxidative stress, chronic inflammation, insulin resistance, and dysregulation of the gut–liver axis. Currently, there remains a lack of effective and long-term safe therapeutic strategies for MASLD, necessitating the development of novel interventions. Plant-derived exosome-like nanovesicles (PELNs) represent naturally secreted nanoscale vesicles derived from plant cells. Their advantages, including extensive availability, high biocompatibility, low immune activation, remarkable stability, and convenient oral administration, make them attractive platforms for therapeutic delivery. PELNs can not only encapsulate natural bioactive compounds such as polyphenols, alkaloids, terpenoids, and polysaccharides but also serve as drug delivery vehicles to achieve liver-targeted transport and synergistic therapy. Current evidence for PELNs in MASLD is predominantly preclinical. In vitro studies have provided mechanistic insights into their effects on lipid metabolism, oxidative stress, inflammatory signaling, and hepatocellular injury, whereas animal studies have demonstrated improvements in hepatic steatosis and related metabolic abnormalities for selected PELNs. A smaller number of studies have investigated tissue distribution, oral uptake, or preliminary biosafety. However, systematic pharmacokinetic, long-term toxicological, and target-species clinical evidence remains insufficient. Accordingly, the therapeutic effects discussed in this review should be interpreted primarily as preclinical findings, and the applicability of PELNs in veterinary practice remains to be established.