Adaptation strategies and resilience mechanisms of the kidney in min pigs under long-term cold stimulation.

The Min pig, a unique local breed in northeastern China, exhibits exceptional cold resistance. However, the renal adaptive mechanisms underlying this trait under long-term cold stimulation remain unclear. This study investigated the effects of long-term cold stimulation on renal structure, antioxidant function, purine metabolism, programmed cell death, and mitochondrial dynamics in Min pigs. The results showed that long-term cold stimulation led to mild morphological changes in the kidneys of Min pigs, as evidenced by pathological sections and ultrastructural analysis. Concurrently, long-term cold stimulation inhibited GSH-Px activity in the kidney and partially impaired the antioxidant capacity. Intriguingly, long-term cold stimulation did not significantly alter the protein levels of major inflammatory factors in the kidney, while IL-2 mRNA expression was increased. Notably, long-term cold stimulation suppressed mRNA expression of CNT1 and ENT2 and promoted mRNA expression of URAT1 in the kidney. At the same time, uricase levels were markedly increased and 5'-NT levels were significantly decreased in the kidney, which may have contributed to the downward trend of UA levels in Min pigs. Surprisingly, long-term cold stimulation does not activate pyroptosis, apoptosis and mitophagy pathways in the kidney of Min pigs. Moreover, long-term cold stimulation increased the expression of OPA1 mRNA in the kidney. In summary, long-term cold stimulation induced mild morphological changes in the kidneys of Min pigs. Simultaneously, the kidney cold adaptation mechanism is triggered, renal purine metabolism is readjusted, and mitochondrial fusion is facilitated. This contributes to mitigating the negative effects of long-term cold stimulation on Min pigs.