Extreme high-temperature events driven by global climate change are occurring with increasing frequency, posing a serious threat to the stability of aquatic ecosystems. The Tibetan schizothoracin (Gymnocypris eckloni), a cold-water fish species endemic to the Qinghai–Tibet Plateau, is highly sensitive to temperature fluctuations and serves as an ideal model for studying the effects of climate change on fish. As a key organ for fish to perceive environmental changes, the gills’ comprehensive response mechanism has not yet been fully elucidated. This study investigated the effects of acute heat stress on the gill tissue of G. eckloni. The results showed that acute heat stress caused severe histopathological damage in the gills, including lamellar curling, epithelial cell detachment, and edema, with a significant increase in apoptosis. Biochemical analysis revealed elevated levels of cortisol, glucose, and ATPase activity in serum, as well as increased MDA content and CAT activity in the gills. Transcriptomic analysis identified 2304 DEGs. Upregulated DEGs were significantly enriched in pathways related to inflammatory response, TNF signaling, ferroptosis, and apoptosis, while downregulated DEGs were primarily involved in peroxisome metabolism, cell cycle, and steroid biosynthesis. This study confirms that acute heat stress induces structural damage and functional impairment in the gills by activating inflammatory and apoptotic pathways and disrupting redox homeostasis. It elucidates the immediate molecular and physiological responses of G. eckloni gills to acute heat stress. Follow-up experiments will be conducted at multiple time points, across different temperature gradients, and under chronic stress conditions to gain a more comprehensive understanding of the adaptive potential of high-altitude fish to climate warming, thereby providing a scientific basis for the development of conservation strategies.

Aeromonas veronii (A. veronii) is ubiquitous in aquatic habitats and infects diverse aquatic animals, causing high mortality and heavy economic losses in aquaculture. In this study, we initially isolated a Gram-negative bacterium (Pv001) from the visceral organs of naturally diseased Paracobitis variegatus. Based on morphological, biochemical, and 16S rRNA and gyrB gene sequence analysis, the isolated strain was accurately determined to be A. veronii. Virulence gene screening showed that the strain Pv001 carried multiple virulence genes, including Acg, Act, Alt, Exu, Lip, and Omp. In vitro antimicrobial evaluations revealed that ceftriaxone, chloramphenicol, ciprofloxacin, and tetracycline displayed significant inhibitory effects on Pv001, while ampicillin, penicillin, and lincomycin exhibited no detectable inhibitory action. The artificial challenge of Paracobitis variegatus with the isolated strain Pv001 via intraperitoneal injection reproduced the clinical signs observed in the affected farm, yielding a calculated LD₅₀ of 8.61 × 10⁵ CFU/fish. Histopathological analysis of the diseased fish indicated extensive intestinal mucosal destruction, vacuolar degeneration of liver cells, and localized necrosis, as well as a considerable number of melano-macrophage centers (MMCs) aggregating in the spleen. This study provides a scientific foundation for the prevention and control of epidemics by revealing the pathogenic features of A. veronii illness in P. variegatus.

Background:Disrupted bile acid homeostasis represents a central feature of cholestatic liver injury, for which effective therapeutic options remain limited. Saxifraga umbellulata Hook. f. et Thoms. (SU) has traditionally been used in Tibetan medicine to treat hepatobiliary disorders, yet the pharmacological basis of SU remains unclear. Therefore, this study aimed to evaluate the effects of SU on cholestatic liver injury and explore the regulatory mechanisms underlying these effects.Methods:A mouse model of cholestatic liver injury was established by administering α-naphthyl isothiocyanate (ANIT). The effects of SU were evaluated using serum biochemical measurements, liver histopathology, and targeted profiling of hepatic bile acids. Protein expression associated with farnesoid X receptor (FXR) signaling was assessed by Western blotting in liver and ileal tissues. Representative triterpenoids in the SU extract were further examined using molecular docking and HepG2 cell experiments.Results:SU administration reduced serum markers of hepatocellular injury and cholestasis and lessened hepatic necrosis and inflammatory cell infiltration in ANIT-treated mice. SU also shifted the altered hepatic bile acid profile toward a more balanced state, including partial correction of the disturbed proportions of primary and secondary bile acids. These metabolic changes were accompanied by reduced hepatic CYP7A1 expression and increased expression of BSEP and MRP2. In addition, SU increased ileal FXR and FGF15 expression and hepatic FGFR4 expression, a pattern consistent with coordinated regulation of the intestinal FXR–FGF15/hepatic FGFR4 axis. Meanwhile, molecular docking and HepG2 cell experiments suggested that cucurbitacin IIb and saxifragic acid may contribute to the observed FXR-related responses.Conclusions:SU mitigated ANIT-induced cholestatic liver injury and promoted partial recovery of hepatic bile acid homeostasis. The protective effects of SU were associated with coordinated changes in hepatic and intestinal FXR-related signaling and with reduced inflammatory injury. These results provide experimental evidence supporting the traditional use of SU for hepatobiliary disorders and highlight cucurbitacin IIb and saxifragic acid as potential bioactive triterpenoids.