Background: The spleen is the primary reservoir of immune cells in mammals. Diverse stimuli can disrupt spleen homeostasis, resulting in spleen injury and immune dysfunction. This study employed a porcine model to assess the therapeutic potential of salvianolic acid B (SAB) against lipopolysaccharide (LPS)-induced splenic injury. Methods: Seventy-two male weanling piglets were randomly assigned to one of four groups: CON-SS, SAB-SS, CON-LPS, and SAB-LPS. The CON-SS and CON-LPS groups received a basal diet, while SAB-SS and SAB-LPS groups received a SAB-supplemented diet. After 14 d, the CON-SS and SAB-SS groups received an intraperitoneal injection of sterile saline, whereas the CON-LPS and SAB-LPS groups were injected with LPS. Blood and spleen tissues were harvested 6 h post-injection for biochemical analysis. Results: LPS induced systemic immune disorders in piglets, as evidenced by increased immune organ indices and decreased white blood cell, lymphocyte, and basophil counts in blood (p < 0.05). LPS also caused histoarchitectural disruption, cell apoptosis, oxidative stress, and inflammation in the spleen (p < 0.05). Conversely, SAB improved splenic histopathology and reduced splenic apoptosis and pro-inflammatory mediators in piglets (p < 0.05). SAB significantly mitigated peroxidation accumulation by facilitating the nuclear translocation of nuclear factor erythroid 2-related factor 2 and strengthening the antioxidant system, and inhibited nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) inflammasome activation (p < 0.05). Mechanistically, SAB attenuated LPS-induced splenic oxidative stress and NLRP3 inflammasome activation by restoring mitochondrial structure and function (p < 0.05). Conclusions: This research unveils that SAB alleviates LPS-induced spleen disorder by reinforcing antioxidant system and suppressing NLRP3 inflammasome, highlighting SAB’s potential as a prospective therapeutic agent for spleen disorders.

Due to the strong polarity and volatility of organic acids, there is often a lack of effective quantitative methods for organic acids in vivo or in vitro. This study introduced a robust and scientifically validated LC-MS methodology for quantitatively analyzing six organic acids, encompassing five short-chain fatty acids and lactate, observed in in vitro fermentation and human fecal samples. This method was able to achieve precise quantification through the monitoring of mass-to-charge (m/z) ratios of the deprotonated negative ions. After optimization, a 2:1 (v/v) dichloromethane/acetonitrile mixture was utilized to extract the crude acid mix from fermentation or fecal samples. Subsequently, the organic acids were isolated using 3 mL of 3.5 M ammonium hydroxide solution from mixtures. The calibration curves for six organic acids demonstrated linearity with R² > 0.991 across the concentration ranges of 0.01–5.0 or 0.01–20 mM. The coefficient of variation and accuracy were 2–13% and 95–128%, respectively, which exhibited good precision and sensitivity. Accurate quantification of organic acids would aid in metabolic analysis in bacterial culture supernatants and human fecal matter.

Background/Objectives: Mycoplasma hyopneumoniae (Mhp), porcine circovirus type 2 (PCV2) and porcine reproductive and respiratory syndrome virus (PRRSV) are major contributors to porcine respiratory disease complex (PRDC), causing substantial economic losses. Methods: This study evaluated a commercial PCV2-Mhp bivalent vaccine, Cirbloc^® M Hyo (Vaccine A), containing recombinant PCV2 Cap protein and inactivated Mhp antigen, vs. two reference bivalent vaccines (B and C) in an Mhp challenge model. Eighty-two healthy 3-week-old specific-pathogen-free piglets were randomly allocated to five groups (three vaccinated, unvaccinated challenged control, unvaccinated unchallenged control). Pigs received a single intramuscular vaccination at 3 weeks of age and were challenged intratracheally with virulent Mhp lung homogenate five weeks later. Clinical signs, serology, lung lesions, histopathology, and Mhp DNA detection in lungs were assessed. Results: No vaccine-related adverse reactions occurred. Vaccine A induced earlier and higher Mhp-IgG seroconversion before challenge than reference vaccines. Following challenge, Vaccine A significantly reduced mean lung lesion scores compared with the unvaccinated challenged control (2.28 ± 2.37 vs. 6.56 ± 4.03; p < 0.05), with markedly reduced peribronchiolar inflammation and lymphoid hyperplasia and the lowest Mhp DNA detection rate among challenged groups. Conclusions: Cirbloc^® M Hyo provided enhanced protection against experimental Mhp challenge, as shown by reduced lung lesions and milder histopathological changes, supporting its use for comprehensive PRDC management.