Fig 2: The potential protective mechanisms of DEX in reducing oxidative stress and apoptosis in LPS-induced AKI. LPS could hold back the formation of autophagosome via activating the PI3K/AKT/mTOR pathway, inducing the accumulation of damaged mitochondria. Then ROS and Cyt C released from damaged mitochondria could induce oxidative stress and apoptosis. DEX could inhibit the PI3K/AKT/mTOR pathway to enhance autophagy by a2-AR, reducing oxidative stress and apoptosis. 3-MA could inhibit the effect of DEX on autophagy.

Fig 3: Effects of DEX treatment on the PI3K/AKT/mTOR pathway. (A) Representative blots (a), and densitometry of p-PI3K/PI3K (b), p-AKT/AKT (b), and p-mTOR/mTOR (c) signals. Data are expressed as mean ± SEM (n = 6). **p < 0.01 versus CON group. ##p < 0.01 versus LPS group. &&p < 0.01 versus DEX + LPS group.

Fig 4: The protein analysis of Pi3k/Akt pathway for FSGD in CRF. (A,E) Western blotting of PTEN, PI3K, p-PI3K, AKT, p-AKT and NF-?B in the kidney. [(B–D) and (F–H)] The relative expression concentration analysis for PTEN, PI3K, p-PI3K, AKT, p-AKT and NF-?B in the kidney. Compared with the normal group, *p < 0.05, **p < 0.01; versus normal group; ## p < 0.01, # p < 0.05, compared with the model group, respectively.