To investigate whether Salvia miltiorrhiza hydrophilic extract (SMHE) has the ability to ameliorate oxidative stress in diabetic patients with chronic heart disease (CHD), 62 patients with CHD were recruited. These patients were assigned randomly into two groups: (1) placebo group receiving hypoglycemic therapy; (2) treatment group receiving hypoglycemic therapy plus SMHE. The biological markers related to oxidative stress were measured to determine the effect of treatment. Thirty patients in the placebo group and 24 patients in the treatment group were followed to completion in this study. Overall, the malondialdehyde (MDA) level at day 30 in the treatment group was significantly lower than in the placebo group. However, no significant difference in the serum antioxidant enzymes activities was observed between the groups. At day 60, the serum glutathione (GSH) level, superoxide dismutase (SOD), Paraoxonase (PONase) and glutathione reductase (GSSG-R) activities increased markedly in the treatment group compared with the placebo group. There was no significant difference in the level of lipid profile between the two groups. This study indicated that SMHE clearly reduced oxidative stress in diabetic patients with CHD.

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The aim of this pilot study was to investigate whether the administration of Salvia miltiorrhiza hydrophilic extract (SMHE) reduced the level of soluble vascular cell adhesion molecule-1 (sVCAM-1) and von Willebrand factor (vWF) in diabetic patients with coronary heart disease (CHD). Sixty-two diabetic patients with CHD were recruited and randomly assigned into placebo and treatment groups. Patients were given SMHE for 60 days. Levels of sVCAM-1, vWF and oxidative low density lipoprotein (oxLDL) were determined by using enzyme linked immunosorbent assay (ELISA). The results showed that the levels of VCAM-1 and vWF positively correlated with the level of oxLDL in diabetic patients with CHD. Levels of sVCAM-1 and vWF in serum were reduced significantly in patients receiving SMHE treatment at day 60 in comparison with the baseline. Administration of SMHE also led to a clear decrease in the levels of oxLDL in diabetic patients with CHD. In summary, this study suggests that SMHE has a potential protective effect on the development of diabetic cardiovascular disease.

Advanced glycation end products (AGEs) play an important role in the onset of diabetic retinopathy. Therefore, in the current study, we investigate whether and how Tanshinone IIa (Tan IIa) from Salvia miltiorrhiza protects bovine retinal endothelial cells (BRECs) against methylglyoxal (MGO) mediated cell dysfunction. The results showed that MGO reduced cell viability in dose dependent manner. The treatment of Tan IIa (50 µM) significantly improved cell viability induced by MGO in BRECs. MGO increased cellular reactive oxygen species formation and cellular nitric oxide (NO) level; enhanced nox1 and iNOS mRNA levels; inhibited prdx1 mRNA level. The treatment of Tan IIa effectually ameliorated cellular oxidative stress. Exposure of MGO resulted in mitochondrial fission and decrease of opa1 and mfn1. No significant difference in mRNA levels of mfn2 and drp1 was detected between MGO and medium. Tan IIa reduced mitochondrial fragmentation, enhanced the mRNA levels of mfn1 and opa1 in MGO cultured BRECs. The short time exposure of cellular antioxidatants, dimethylthiourea (10mM) and tiron (10mM) had no effect on mitochondrial fission although they ameliorated cellular reactive oxygen species level. Moreover, overexpression of GLO1 increased key proteins of mitochondrial fusion, including OPA1 and MFN1 in BRECs cultured with MGO. However, inhibition of GLO1 by siRNA abolished the effect of Tan IIa on induction of mitochondrial fusion in MGO cultured BRECs. In conclusion, MGO caused the injury of retinal endothelial cells through induction of mitochondrial dysfunction and mitochondrial fission, the treatment of Tan IIa ameliorated mitochondrial dysfunction and fission induced by AGEs through enhancing GLO1.

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