To assess the influence of a high-dose of vitamin B₆ on severe trauma-induced hepatic stress injury (HSI).

HepG2 cells were cultured with final concentrations of vitamin B₆ ranging from 0 to 4 mmol/L for 24 hours, and the IC50 was determined using the CCK8 assay. Male SD rats were selected and randomized into sham group (n=30), sham+ B₆ group (n=30), trauma group (n=30), and trauma+ B₆ group (n=30) using a random number table. At each time point (12、24、36、48 adn 72 h), there were 6 rats in ecah group. Severe multiple injuries were induced, including abdominal injury, bilateral femoral fractures, and unilateral cranial injury, followed by 20% blood loss and fluid resuscitation. Sham groups received arterial puncture and fluid resuscitation without severe injuries. Rats were euthanized at 12, 24, 36, 48, and 72 hours post-injury, and blood samples and liver tissues were collected. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured using an automatic biochemical analyzer. Pathological changes in liver tissues were observed through hematoxylin-eosin (HE) staining, oil red staining, and transmission electron microscope.

The IC50 value of vitamin B₆ for HepG2 cells was determined to be 4 mmol/L, confirming the safe dosage range used in this study. In comparison to sham groups, the serum ALT and AST levels in rats gradually increased at 12, 24, and 36 hours post-trauma and declined thereafter. The trauma+ B₆ group exhibited significantly lower ALT levels at 12, 36, and 72 hours [ (121.78±2.38) U/L vs. (177.41±6.00) U/L; (299.05±18.54) U/L vs. (447.03±22.02) U/L; (35.01±1.47) U/L vs. (48.32±4.79) U/L, all P<0.05]. Similarly, the trauma+ B₆ group showed significantly lower AST levels at 12, 24, 36, and 48 hours [ (601.52±17.27) U/L vs. (726.66±22.20) U/L; (619.44±45.05) U/L vs. (779.81±27.29) U/L; (672.36±16.50) U/L vs. (871.61±20.23) U/L; (133.26±19.11) U/L vs. (285.13±31.28) U/L, all P<0.05]. HE staining revealed that the injured area in rat livers was concentrated around the central vein and portal vein at 12 hours post-trauma, progressed to periportal hepatocytes and sinusoids at 24 and 36 hours, and became fixed and gradually reduced in size at 48 and 72 hours. The trauma+ B₆ group exhibited significantly reduced liver cell damage at all time points. Oil red staining at 36 hours post-trauma showed a significant downregulation of lipid droplet quantity and diameter in liver cells of the trauma+ B₆ group compared to the trauma group. Transmission electron microscopy at 36 hours post-trauma revealed reduced mitochondrial swelling, restored cristae, visible rod-shaped mitochondria, and a decrease in lipid droplets, autophagic precursors, autophagosomes, and autolysosomes in the trauma+ B₆ group compared to the trauma group.

High-dose vitamin B₆ can alleviate hepatic edema, degeneration, and microvesicular steatosis, reducing severe trauma-induced HSI. Additionally, the 36-hour time point post-trauma appears to be a critical juncture in the progression of HSI following severe trauma.