This experiment aimed to explore whether young internal environment could alleviate renal interstitial fibrosis induced by kidney ischemia-reperfusion injury (IRI) in elderly mice.

Male C57BL/6 mice aged 12 weeks and 22 months were used to establish youth-youth, youth-old, and old-old parabiosis models. Three weeks after establishment of the parabiosis models, the recipient mice, as well as young and old mice without parabiosis received induction of renal unilateral IRI (uIRI). The uIRI mice with and without parabiosis were divided into 5 groups, including youth-youth parabiosis uIRI group (Y-IP uIRI group), youth-old parabiosis uIRI group (O-HP uIRI group), old-old parabiosis uIRI group (O-IP uIRI group), youth uIRI group (Y uIRI group), and old uIRI group (O uIRI group). Blood and renal tissue samples were collected at 1 day, 3 days, and 14 days after surgery for tests of serum creatinine and blood urea nitrogen. The pathological changes of kidneys were observed with Sirius red staining. Fibrotic markers such as α-smooth muscle actin (α-SMA), vimentin, and type I collagen (COL-Ⅰ) were detected with Western blotting.

The Y-IP uIRI group had its renal function to baseline level at day 14, while the O-IP uIRI group and the O-HP uIRI group did not have their renal function restore to baseline level. However, the renal function of O-HP uIRI group was significantly better than that of the O-IP uIRI group. At day 14, the renal fibrosis of both the O-IP uIRI group and O-HP uIRI group significantly increased compared with that of the Y-IP uIRI group. Moreover, the renal interstitial fibrosis of O-HP uIRI group significantly reduced compared with that of the O-IP uIRI group. Western blot results showed that renal fibrosis markers of α-SMA, vimentin, and Col-Ⅰ had similar changes.

Young internal environment could alleviate the renal interstitial fibrosis induced by IRI in the elderly mice so as to delay the progression of AKI-CKD.