Objective To establish a simple diabetic peripheral neuropathy (DPN) rat model with the high fat-fed in GK rats. Methods A total of 30 GK rats (7-8 weeks) were fed with high-fat diet to establish the DPN model. Thirty normal Wistar rats were fed with ordinary diet (control group). The blood-sugar value, body mass, water-intake and food-intake were monitored every week in two groups. The serum level of glycosylated hemoglobin, the right sciatic nerve conduction velocity were detected at 8, 12 and 16 weeks respectively. The left sciatic nerve was used for HE and TUNEL staining. Results The manifestations of polydipsia, polyphagia and growth retardation were gradually appeared in GK rats. After 12 and 16 weeks, the blood-sugar and glycosylated hemoglobin were significantly increased in GK rats compared with those of normal Wistar rats (P < 0.01). The sensory nerve conduction velocity decreased obviously (P < 0.01). And motor nerve conduction velocity showed a certain decline trend (12 week P < 0.05,16 week P > 0.05). The sciatic nerve pathological features and Schwann cell apoptosis suggested that the model of DPN was successfully established (apoptosis index, P <0.01). Conclusion GK rats fed by high-fat diet are the satisfactory models of the DPN in experimental research. And 12-week is a suitable and economical time for molding.

Heterotypic cell-in-cell structures (heCICs) are closely related to tumor development and progression, and have become a new frontier in life science research. Ras-related C3 botulinum toxin substrate 1 (Rac1) belongs to the classic Rho GTPase, which plays a key role in regulating the cytoskeleton and cell movement. To investigate the role and mechanism of Rac1 in the formation of heCICs, tumor cells and immune killer cells were labeled with cell-tracker, respectively, to establish the heCICs model. Upon treatment with the Rac1 inhibitor NSC23766, the formation of heCICs between tumor and immune cells was significantly reduced. The plasmid pQCXIP-Rac1-EGFP constructed by gene cloning was packaged into pseudoviruses that subsequently infect tumor cells to make cell lines stably expressing Rac1. As a result, the formation of heCICs was significantly increased upon Rac1 overexpression. These results demonstrated a promotive role of Rac1 in heCICs formation, which may facilitate treating cell-in-cell related diseases, such as tumors, by targeting Rac1.