Abstract
OBJECTIVE: Intestinal barrier disruption is central to heat stroke (HS) pathogenesis. Probiotics such as Bifidobacterium may offer protection. This study aimed to investigate the mechanism by which Bifidobacterium preserves intestinal mucosal barrier integrity in a rat model of HS. METHODS: A total of 32 rats received Bifidobacterium (Con-BB and HS-BB) or saline (Con-NS, HS-NS) for 14 days. HS was induced via forced running in heat/humidity. Serum markers (tissue damage, inflammation, and barrier injury), histopathology, and gut microbiota were analyzed. RESULTS: Compared with the HS-NS group, the HS-BB group showed a marked reduction in the characteristic histopathological injuries of the liver, kidney, and intestine, along with increased expression of ileal ZO-1 and colonic Occludin proteins ( P < 0.05). Serum biomarkers reflecting tissue damage (total bilirubin and lactate dehydrogenase) and inflammation-6 were all significantly decreased in the HS-BB group ( P < 0.05). Gut microbiota composition differed markedly between the HS-BB and HS-NS groups; Psychrobacter abundance was significantly reduced in HS-BB and identified as a key discriminator. Furthermore, expression of heat shock proteins (HSPs) (colonic HSP27 and HSP70) was significantly elevated in HS-BB compared with the HS-NS group. Strong positive correlations existed between ileal Occludin and HSP27 ( r = 0.886, P = 0.019), and ileal ZO-1 and HSP70 ( r = 0.829, P = 0.042). CONCLUSIONS: Bifidobacterium pretreatment conferred significant multiorgan protection and reduced systemic inflammation in HS rats. The core protective mechanism involves preserving intestinal mucosal barrier function. Maintaining intestinal mucosal barrier integrity may represent a promising strategy for the prevention of HS and the mitigation of associated systemic inflammatory responses and multiple organ dysfunction syndrome.