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Fig. 6 | Molecular Medicine

Fig. 6

From: Fibroblast growth factor 21 attenuates salt-sensitive hypertension-induced nephropathy through anti-inflammation and anti-oxidation mechanism

Fig. 6

rhFGF21 activated renal AMPK and changed nuclear abundance of NF-κB p65 and Nrf2 in SSHN mice. Eight-week-old male FGF21 WT mice were treated with DOCA-salt or sham operation as controls, followed by intraperitoneal administration of recombinant human FGF21 (rhFGF21, 500 μg/kg/day body weight) or same volume of 0.9% normal saline. Kidney tissues were harvested at 8 days after intervention. a The protein expression levels of AMPK and phosphorylated AMPK (p-AMPK) were measured by Western blot using anti-AMPK and anti-p-AMPK antibodies. GAPDH was used as the internal control and the relative ratio of p-AMPK/AMPK was quantified and the normalized values were indicated in the histogram. b Western blot results for protein levels of NF-κB p65 in nuclear fractions in the kidney tissues of each group and statistical analysis of the nuclear abundance of NF-κB p65. Lamin B was used as the internal control. c The levels of nuclear accumulation of Nrf2 in kidney tissues of each group were detected by Western blot analysis and quantification of the nuclear protein expression of Nrf2 in nuclear fractions was analyzed by Image J. Lamin B was used as loading and normalization control. Data are presented as Mean ± SD, n = 6 mice/group. *P < 0.05, **P < 0.01 versus the WT control group; #P < 0.05, ##P < 0.01 versus the WT-DOCA group

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