Human Tissue Kallikrein 1 Improves Erectile Dysfunction of Streptozotocin-Induced Diabetic Rats by Inhibition of Excessive Oxidative Stress and Activation of the PI3K/AKT/eNOS Pathway.
Yang LuanKai CuiZhe TangYajun RuanKang LiuTao WangZhong ChenShao-Gang WangJi-Hong LiuPublished in: Oxidative medicine and cellular longevity (2020)
hKLK1 preserves erectile function of DM rats through its antitissue excessive OS, apoptosis, and fibrosis effects, as well as activation of the PI3K/AKT/eNOS/cGMP pathway in the penis. Moreover, hKLK1 promotes relaxation and prevents high glucose-induced injuries of CSMC mediated by EC-CSMC crosstalk.
Keyphrases
- diabetic rats
- oxidative stress
- endothelial cells
- high glucose
- dna damage
- ischemia reperfusion injury
- induced apoptosis
- weight gain
- nitric oxide
- pi k akt
- nitric oxide synthase
- type diabetes
- cell death
- mouse model
- body mass index
- physical activity
- high fat diet
- induced pluripotent stem cells
- cell cycle arrest
- cell proliferation
- glycemic control