高脂血症易感(WSHc)大鼠 z-bo 2020-11-09 349

　　Objective To observe the pathogenesis and pathological characteristics of spontaneous hindlimb paralysis rats in the hyperlipidemia susceptible (WSHc) rat population, and preliminarily study its pathogenesis, and explore its application and scientific research value.

　　Methods In the WSHc rat population cultivated in our center, 8 spontaneous hindlimb paralysis rats and 8 rats from the same family with no paralysis symptoms of the same age were fed with ordinary diet and high-fat diet, respectively. Susceptibility to hyperlipidemia; MRI and histopathology were used to observe the central neuropathy in different parts of rats with hindlimb paralysis, and TUNEL immunohistochemical method was used to observe the level of apoptosis; RT-PCR was used to detect the central nervous system in different parts Caspase-1 and IL-1β gene expression, and use Western Blot method to detect protein expression.

　　Results Both male and female WSHc rats with paralyzed hind limbs can develop the disease. The sensitivity to high-fat diet was not significantly different from that of WSHc rats without hindlimb paralysis. Magnetic resonance imaging showed no significant lesions in the brain and cerebellum, and histopathology showed paralysis of the hind limbs. A large number of inflammatory cell infiltration and positive expression of TUNEL in the middle and posterior segment of the spinal cord of WSHc rats, compared with non-paralyzed WSHc rats, the expression of Caspase-1 and IL-1β genes in the posterior segment of the spinal cord was significantly increased (P<0.05, P< 0.01), and protein expression also increased significantly (P<0.05).

　　Conclusion Spontaneous hindlimb paralysis in hyperlipidemia-susceptible WSHc rats is a progressive lesion, and its onset site is located in the middle and posterior part of the spinal cord. The pathological features are inflammatory cell infiltration and neuronal cell degeneration and apoptosis. Its pathogenesis may be related to Caspase-1. Overactivation is related.