β-Caryophyllene (BCP) is a bicyclic sesquiterpene compound that has anti-diabetic activity. However, the effect of BCP on diabetic nephropathy (DN) remains unclear. Here, we aimed to evaluate the potential role of BCP in high glucose (HG)-induced glomerular mesangial cells (MCs). MCs were maintained under HG condition to simulate DN in vitro. Our results showed that BCP inhibited HG-induced cell proliferation, ROS production and NADPH oxidase (NOX) 2/4 expression. BCP exhibited anti-inflammatory activity with decreased levels of TNF-α, IL-1β, IL-6 in HG-induced MCs. Moreover, BCP treatment suppressed the HG-induced secretion of fibronectin (FN) and collagen IV (Col IV) in MCs. Furthermore, BCP suppressed the NF-κB activation and enhanced the Nrf2 activation in HG-induced MCs. However, inhibition of Nrf2 attenuated the protective effects of BCP on HG-induced MCs, while inhibition of NF-κB enhanced the nephro-protective effects of BCP on MCs. In conclusion, these findings demonstrated that BCP executed protective effects on HG-induced MCs via regulating NF-κB and Nrf2 signaling pathways.

β-石竹烯（BCP）是具有抗糖尿病活性的双环倍半萜烯化合物。但是，BCP对糖尿病性肾病（DN）的作用仍不清楚。在这里，我们旨在评估BCP在高葡萄糖（HG）诱导的肾小球系膜细胞（MCs）中的潜在作用。后MC HG条件下保持以模拟DN体外。我们的结果表明，BCP抑制HG诱导的细胞增殖，ROS产生和NADPH氧化酶（NOX）2/4表达。BCP在HG诱导的MCs中表现出抗炎活性，并降低TNF-α，IL-1β，IL-6的水平。此外，BCP处理可抑制HG诱导MCs分泌纤连蛋白（FN）和胶原IV（Col IV）。此外，BCP抑制了HG诱导的MC中的NF-κB活化并增强了Nrf2活化。然而，抑制Nrf2减弱了BCP对HG诱导的MCs的保护作用，而抑制NF-κB增强了BCP对MCs的肾脏保护作用。总之，这些发现表明，BCP通过调节NF-κB和Nrf2信号通路对HG诱导的MC发挥保护作用。