Hibiscus attenuates renovascular hypertension–induced aortic remodeling dose dependently: the oxidative stress role and Ang II/cyclophilin A/ERK1/2 signaling

Abstract

Introduction: The high levels of angiotensin II (Ang II) can modify the vascular tone, enhance vascular smooth muscle cells (VSMCs) proliferation and hypertrophy and increase the inflammatory cellular infiltration into the vessel wall. The old herbal nonpharmacological agent, Hibiscus (HS) sabdariffa L has multiple cardioprotective impacts; thus, we investigated the role of HS extract in amelioration of renovascular hypertension (RVH)-induced aortic remodeling.Materials and methods: Thirty-five rats (7/group) were randomly allocated into 5 groups; group: I: Control-sham group, and RVH groups; II, III, IV, and V. The rats in RVH groups were subjected to the modified Goldblatt two-kidneys, one clip (2K1C) for induction of hypertension. In group: II, the rats were left untreated whereas in group III, IV, and V: RVH-rats were treated for 6 weeks with low dose hibiscus (LDH), medium dose hibiscus (MDH), and high dose hibiscus (HDH) respectively.Results: We found that the augmented pro-contractile response of the aortic rings was ameliorated secondary to the in-vivo treatment with HS dose dependently. The cyclophilin A (CyPA) protein levels positively correlated with the vascular adhesion molecule-1 (VCAM-1) and ERK1/2, which, in turn, contribute to the reactive oxygen species (ROS) production. Daily HS intake modified aortic renovation by enhancing the antioxidant capacity, restraining hypertrophy and fibrosis, downregulation of the metastasis associated lung adenocarcinoma transcript (MALAT1), and cyclophilin A (CyPA)/ERK1/2 levels.Discussion: Adding to the multiple beneficial effects, HS aqueous extract was able to inhibit vascular smooth muscle cell proliferation induced by 2K1C model. Thus, adding more privilege for the utilization of the traditional herbal extracts to attenuate RVH-induced aortopathy.

Peptides from Harpadon nehereus Bone Ameliorate Angiotensin II-Induced HUVEC Injury and Dysfunction through Activation of the AKT/eNOS and Nrf2 Pathway

“…This experiment explored whether KA-8 and PG-7 could reverse the Ang II-induced increase in the level of ROS in HUVECs. As shown in Figure , the Ang II group showed a stronger fluorescence state than the Con group, which was consistent with previous findings . After treatment with KA-8 and PG-7, the intracellular fluorescence intensity decreased significantly and the PG-7 group had the best effect.…”

“…As shown in Figure 2 , the Ang II group showed a stronger fluorescence state than the Con group, which was consistent with previous findings. 10 After treatment with KA-8 and PG-7, the intracellular fluorescence intensity decreased significantly and the PG-7 group had the best effect. The results showed that two peptides, especially PG-7, could inhibit the production of ROS induced by Ang II in HUVEC, thereby reducing the oxidative damage caused by ROS.…”