To elucidate the effects of cultivar and harvest month on the phenolic content and antioxidant activity of mulberry leaves, four major phenolics, including chlorogenic acid (ChA), benzoic acid (BeA), rutin (Rut) and astragalin (Ast), were quantified using an HPLC-UV method. Leaves from six mulberry cultivars, collected from April to October, were analyzed. The antioxidant activity of mulberry leaves was assessed by ferric reducing antioxidant power (FRAP), hydroxyl radical scavenging activity (HSA) and superoxide radical scavenging activity (SSA) assays. The results showed that the total values of the four phenolic compounds ranged from 2.3 dry weight (DW) to 4.2 mg/g DW, with ChA being the major compound. The mean total phenol (TP) content of the six cultivars ranged from 30.4 equivalents (GAE) mg/g DW to 44.7 GAE mg/g DW. Mulberry leaves harvested in May had the highest TP content. Moreover, the antioxidant activities of mulberry leaves harvested from April to October differed noticeably. In general, Kq 10 and May were considered to be a better cultivar and harvest month concerning phenolic content and antioxidant activity, respectively.

Hyperglycemia is associated with increased risk of type 2 diabetes, partially due to increases in oxidative stress. Phenolics in mulberry leaves (MLP) may protect tissues from hyperglycemia‐induced oxidative damage. We examined the effect of MLP on hyperglycemia‐induced oxidative damage in hepatic HepG2 cells. HepG2 were treated with glucose (5.5 or 50 mM) with or without MLP at 10 or 100 μM GAE. Hyperglycemia‐induced oxidative damage in HepG2 was demonstrated by a 666% increase in O2.− production at 0.5 h, 400% increase in malondialdehyde (MDA) at 24 and 48 h, mitochondrial membrane hyperpolarization (MMHP) at 2 h followed by depolarization, and 474% increase in nucleus NFκB‐P65 at 4 h relative to the control cells (P ≤0.05). Both MLP doses inhibited hyperglycemia‐induced O2.− production by 40%. Hyperglycemia‐induced MDA production at 24 h was diminished by 34 and 54% by MLP at 10 and 100 μM, respectively. MLP treatment protected HepG2 cells from hyperglycemia‐induced MMHP in a dose‐dependent manner with the highest dose maintaining mitochondrial polarization status. MLP at 10 μM inhibited 35% hyperglycemia‐induced NFκB‐P65 translocation and at 100 μM completely prevented the NFκB activation. Our data show that MLP in vitro protects hepatoctyes from hyperglycemia‐induced oxidative damage.