【Animal Modeling】-Study on the characteristics of spontaneous hindlimb paralysis in hyperlipidemia susceptible (WSHc) rats

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

  Methods In the WSHc rat population cultivated in our center, 8 rats with spontaneous hindlimb paralysis and 8 rats from the same family without paralysis symptoms of the same age were fed with normal diet and high-fat diet, respectively. Hyperlipidemia susceptibility; MRI and histopathology were used to observe central neuropathy in different parts of hindlimb paralyzed rats, and TUNEL immunohistochemistry was used to observe the level of apoptosis; RT-PCR was used to detect central nervous system in different parts The expression of Caspase-1 and IL-1β gene was detected by Western Blot.

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

  Conclusions Spontaneous hindlimb paralysis in hyperlipidemia-susceptible WSHc rats is a progressive disease, the onset site is located in the middle and posterior segment of the spinal cord, and its pathological features are inflammatory cell infiltration and neuronal cell degeneration and apoptosis. over-activated.