Preliminary Study On The Effect Of STRN On The Proliferation And Apoptosis Of Thoracic Aortic Vascular Smooth Muscle Cells In Salt-sensitive Hypertensive Rats Based On PI3K/Akt Pathway

Objective: Preliminary study on the effect of striatin(STRN)on the proliferation and apoptosis of thoracic aortic vascular smooth muscle cells(VSMCs)in rats with salt-sensitive hypertension(SSH)by regulating PI3K/Akt signaling pathway.Methods: The 7-week-old male SPF Wistar rats(n=21)were acclimated to feeding for 1 week,and their basal blood pressure was measured.They were randomly divided into control group(CON group)(n=7)and high-salt feeding group(n=14),respectively.Rats were fed with normal salt(containing 0.4% Na Cl)and high-salt(containing 8.0% Na Cl)pelleted diets.During the period,the blood pressure of the tail of the rats was measured.The measured systolic blood pressure ≥ 140 mm Hg was judged as SSH(n=7)rats.The primary thoracic aortic smooth muscle cells of the rats in the SSH group and the SSH group were isolated and cultured,identified by immunofluorescence,and the background expression of STRN was detected by q RT-PCR.Akt inhibitor(LY294002)treatment,divided into control group(Control),overexpression empty group(NC),overexpression group(STRN),overexpression empty expression + inhibitor group(NC + LY294002)and overexpression +inhibition group In the drug group(STRN+LY294002),the cell cycle and apoptosis were detected by flow cytometry,the cell proliferation activity was detected by CCK-8 method,and the protein expressions of STRN,PI3 K,Akt,p-PI3 K and p-Akt were detected by Western blot.Results: 1.Compared with the control group(CON group)rats,the STRN expression in the salt-sensitive hypertensive rat group(SSH group)was decreased(P<0.05).2.Compared with the 0 μM concentration group of PI3K/Akt inhibitor,the cell viability in the 5 μM,10 μM,20 μM,30 μM and 40 μM concentration groups was significantly decreased(all P<0.05).Cell viability was inhibited with increasing inhibitor concentration.3.Compared with the Control group,the G0/G1 phase of the NC group and the STRN group was significantly decreased(all P<0.05),and the G0/G1 phase of the NC+LY294002 group and the STRN+LY294002 group was significantly increased(all P<0.05);the S phase of the NC group and the STRN group was significantly increased(all P<0.05),the S phase of the NC+LY294002 group and the STRN+LY294002 group was significantly decreased(all P<0.05);the G2/M phase of the NC+LY294002 group was significantly decreased(P<0.05),indicating that the NC+LY294002 group and the STRN+LY294002 group were blocked in G0/G1 phase.4.Compared with the Control group,the apoptotic rate was significantly decreased in the NC group(P<0.05),and significantly increased in the NC+LY294002 group and the STRN+LY294002 group(all P<0.05).Compared with the Control group,the cell proliferation rates in the NC group,the STRN group,the NC+LY294002 group,and the STRN+LY294002 group were increased significantly(all P<0.05).Compared with the NC group,the cell proliferation rate of the NC+LY294002 group was significantly decreased(P<0.05).Compared with the NC group,the proliferation rate of cells in the STRN group increased(P<0.05).Compared with the STRN group,the cell proliferation rate of the NC+LY294002 group was significantly decreased(P<0.05).This indicated that the overexpression of STRN could inhibit cell apoptosis and promote cell proliferation.5.Compared with Control group,p-Akt 、 p-PI3 K and STRN were significantly up-regulated in STRN group(all P<0.05),and p-Akt and p-PI3 K were significantly up-regulated in NC+LY294002 group and STRN+LY294002 group(all P<0.05).Compared with NC group,the expression of STRN in STRN group was significantly up-regulated(P<0.05),and the expression of p-Akt and p-PI3 K in STRN group,NC+LY294002 group and STRN+LY294002 group were significantly up-regulated(all P<0.05).Compared with STRN group,the expression of p-Akt and p-PI3 K in NC+LY294002 group was significantly down-regulated(all P<0.05).Conclusion: STRN may promote the proliferation of thoracic aortic vascular smooth muscle cells in salt-sensitive hypertensive rats and inhibit the apoptosis of thoracic aortic vascular smooth muscle cells in salt-sensitive hypertensive rats by activating the PI3K/Akt signaling pathway.