Aqueous extract of Peristrophe bivalvis leaf alleviates oxidative stress in L-NAME-induced hypertensive rats

Hypertension, known as the silent killer, is associated with several complications, of which oxidative stress is thought to be one of the major fundamental mechanisms causing these complications. Conversely, Peristrophe bivalvis (PB) (L.) Merr. is utilized in alternative medicine to address hypertension, diabetes, and various other conditions. Studies have indicated its blood pressure-lowering effect in different models of hypertension; furthermore, its in vitro antioxidant activities have also been reported. However, there is a paucity of data regarding its in vivo antioxidant properties. This research investigated the impact of the aqueous extract of PB leaf (APBL) on oxidative stress induced by hypertension in rats, which was triggered by NG-Nitro-L-arginine methyl ester (L-NAME). Thirty male Wistar rats were randomly allocated to six different groups (n = 5 each): control group (10 mL/kg distilled water D10), hypertensive sacrificed in week 8 group (euthanized in the eighth week), untreated hypertensive group (60 mg/kg L-NAME L60 + D10, H), hypertensive recovery group (D10), standard drug-hypertensive group (L60 + 10 mg/kg ramipril), and APBL-hypertensive group (L60 + 200 mg/kg APBL APBLH). Blood pressure and serum levels of malondialdehyde, superoxide dismutase, glutathione, angiotensin II, and endothelin 1 were measured. Heart histology was examined to determine L-NAME hypertension severity. The results indicated a notable reduction in blood pressure (SBP: 148 ± 2.28 vs. 196 ± 4.47; DBP: 110 ± 6.69 vs. 158 ± 6.22; and MAP: 171 ± 4.30 vs. 123 ± 4.66 mm Hg, p < 0.05), malondialdehyde (1.40 ± 0.14 vs. 9.26 ± 1.06 µM/mg protein, p < 0.05), angiotensin II (29.40 ± 1.34 vs. 51.34 ± 2.28 pmol/L, p < 0.05), and endothelin-1 (86.42 ± 5.88 vs. 122.60 ± 6.37 pg/mL, p < 0.05) levels in APBLH when compared to H. The levels of superoxide dismutase (2.38 ± 0.34 vs. 0.29 ± 0.05 U/mg protein, p < 0.05) and glutathione (1.32 ± 0.47 vs. 0.30 ± 0.10 mM/mg protein, p < 0.05) were markedly elevated in APBLH in comparison to H. Furthermore, the APBLH group demonstrated an improvement in heart histopathology compared to the H group. Conclusively, the results of this research indicate that APBL significantly mitigated the oxidative stress caused by hypertension in rats. This antioxidant effect is likely due to its capacity to lower levels of endothelin-1 and angiotensin II, both of which are recognized for their role in inducing oxidative stress by augmenting the formation of reactive oxygen species.