The present study examined the effects of procyanidin B2 (PB2) on L-NAME (nitric oxide synthase inhibitor)-induced hypertensive nephropathy. After 4 weeks of treatment with daily PB2 supplementation, lower blood pressure levels were observed in rats. The potential mechanisms were combined with amelioration of renal function impairment. The L-NAME–induced renal histological damage were reduced by PB2 treatment, which showed similar protective tendency in kidney injury molecule–1, nephrin, fibronectin and α–smooth muscle actin protein expression. This appears to be due to PB2 inducing a less pronounced generation of renal reactive oxygen species and inflammatory mediators than in the model group. Downregulation of Ang II type 1 receptor and NADPH oxidase subunit (NOX4, gp91phox and p47phox) played a critical role in the effect of PB2 reducing oxidative stress production. These activities could further support the use of PB2 commercially in food for the prevention of hypertension and its complications.

本研究检查了原花青素B2（PB2）对L-NAME（一氧化氮合酶抑制剂）诱导的高血压肾病的影响。每天补充PB2的治疗4周后，在大鼠中观察到较低的血压水平。潜在的机制与改善肾功能损害相结合。PB2处理可减轻L-NAME诱导的肾脏组织学损伤，在肾脏损伤分子1，肾素，纤连蛋白和α-平滑肌肌动蛋白蛋白表达中显示出相似的保护趋势。这似乎是由于PB2诱导的肾反应性氧种类和炎性介质的产生少于模型组。Ang II 1型受体和NADPH氧化酶亚基（NOX4，gp91phox和p47phox）在PB2减少氧化应激产生的作用中起着关键作用。这些活动可进一步支持PB2在商业上用于预防高血压及其并发症的食品用途。