This exposure may give rise to the proliferation of vascular smooth muscle and result in the incrassation of endothelium with low endothelial cell content, suggesting that hyperlipidemia-induced ED may be the result of vascular blocking and cavernosal ischemia. Our results show similar pathological changes in HFD group, and we find that Phorbol 12,13-dibutyrate cavernous smooth muscle to collagen ratio significantly decreased in BIIAL and BCH groups, seems paradoxical to the others. However, Yes?illi and Iacono et al. demonstrated the content of collagen increased and progressive fibrosis in hyperlipidemia induced ED rabbits and human cavernous tissue after one year observation and follow-up, suggesting that increase in collagen participates the pathology of ED when the modeling period extended. It is appropriate to infer that decrease in cavernous smooth muscle to collagen ratio is mainly depended on the collagen content, which relatively decreases the cavernous smooth muscle expression, in BCH group and the effect is strengthened by BIIAL injury. Azadzoi et al. demonstrated reduced NOS activity may result in the impairment of endothelium-dependent, neurogenic relaxation in cavernosal tissue by balloon de-endothelialization and a high cholesterol diet. In the present study, the expression of nNOS in the BIIAL and BCH groups was significantly decreased compared to the NC group, but the difference was not significant between the BIIAL and BCH groups. Furthermore, the expression of eNOS in the HFD and BCH groups was significantly decreased compared to the NC group, but there was no significant difference found between the HFD and BCH groups. According to a previous study, BCH may not reduce NOS subtype activity like HFD or BIIAL, but instead decrease the activity of NOS collectively. As rats rarely develop atherosclerotic lesions like humans or rabbits, the method successful produced an ED rat model and reduced the model Pristimerin establishment period from 16 weeks to 12 weeks. This method may be a feasible way to establish an ED model. In addition, nNOS and eNOS initiate penile erection and are involved in sustaining the erection. Recently, many studies have associated eNOS and nNOS with the level of erectile function. Accordingly, BCH-induced ED showed lower ICP without recovery, and the NOS levels were consistently lower than normal. Thus, the BCH group may overcome the autocompensation of the BIIAL model and shorten the duration required to establish the HFD model, which further confirms our conclusion that the BCH model mimics the pathophysiology of ED in humans and avoids the drawbacks of traditional ED models. Previous research showed that the serum lipid levels of animals fed a high-fat diet increased with the duration of feeding time and reached a plateau at 4 weeks, but vascular injury lagged.