Background: Danshen (Salviae Miltiorrhizae Radix) and Gegen (Puerariae Lobatae Radix) have been used for treating heart disease for several thousand years in China. It has been found that a Danshen and Gegen decoction (DG) exhibiting an anti-atherosclerosis effect, which improves the patients’ heart function recovery. Pre-treatment with DG was reported to have protective effects on myocardium against ischemia/reperfusion injury. In the present study, we aim to investigate the post-treatment effect of DG on ischemic-reperfusion injuriesex vivoorin vitroand the underlying mechanisms involved.Methods: The rat heart function in an ischemia and reperfusion (I/R) model was explored by examining three parameters including contractile force, coronary flow rate and the release of heart specific enzymes within the heart perfusate.In vitromodel of hypoxia and reoxygenation (H/R), the protective effect of DG on damaged cardiomyocytes was investigated by examining the cell structure integrity, the apoptosis and the functionality of mitochondria.Results: Our results showed that DG significantly improved rat heart function after I/R challenge and suppressed the release of enzymes by damaged heart muscles in a dose-dependent manner. DG also significantly inhibited the death of cardiomyocytes, H9c2 cells, with a H/R challenge. It obviously decreased cell apoptosis, protected the mitochondrial function and cell membrane skeleton integrity on H9c2 cells. The cardio-protection was also found to be related to a decrease in intracellular calcium accumulation within H9c2 cells after I/R challenge.Conclusion: The potential application of DG in treating rat hearts with an I/R injury has been implied in this study. Our results suggested that DG decoction could act as an anti-apoptotic and anti-ion stunning agent to protect hearts against an I/R injury.

Our previous study reported that mesenchymal stem cells (MSCs) accelerated the wound healing process through anti-inflammatory, anti-apoptotic, and pro-angiogenetic effects in a rodent skin excision model. NF3 is a twin-herb formula, which presents similar effects in promoting wound healing. Research focusing on the interaction of MSCs and Chinese medicine is limited. In this study, we applied MSCs and the twin-herb formula to the wound healing model and investigated their interactions. Wound healing was improved in all treatment groups (MSCs only, NF3 only, and MSCs + NF3). The combined therapy further enhanced the effect: more GFP-labelled ADMSCs, collagen I and collagen III expression, Sox9 positive cells, and CD31 positive cells, along with less ED-1 positive cells, were detected; the expressions of proinflammatory cytokine IL-6 and TNF-α were downregulated; and the expression of anti-inflammatory cytokine IL-10 was upregulated. In vitro, NF3 promoted the cell viability and proliferation ability of MSCs, and a higher concentration of protein was detected in the NF3-treated supernatant. A proteomic analysis showed there were 15 and 22 proteins in the supernatants of normal ADMSCs and NF3-treated ADMSCs, respectively. After PCR validation, the expressions of 11 related genes were upregulated. The results of a western blot suggested that the TGFβ/Smad and Wnt pathways were related to the therapeutic effects of the combined treatment. Our study suggests for the first time that NF3 enhanced the therapeutic effect of MSCs in the wound healing model and the TGFβ/Smad and Wnt pathways were related to the procedure.

Ergothioneine (EGT), an active compound in many edible mushrooms, has considerable potential for therapeutic intervention in neurodegenerative diseases. However, whether EGT can safely alleviate symptoms of Parkinson’s disease (PD) and its neurophysiological mechanisms remain unclear. In this study, 6-hydroxydopamine (6-OHDA) mouse model of PD was chosen to mimic the pathological progression observed in the early stages of PD patients. After four weeks of EGT treatment (8 mg/kg/d), there was a significant improvement in motor impairments of 6-OHDA mice with a reduction in dopaminergic neuronal loss in the substantia nigra pars compacta (SNc). Using in vivo multi-electrophysiological recordings, we found that EGT treatment increased the firing rates of neurons in the primary motor cortex (M1) of 6-OHDA mice. In addition, EGT treatment notably reduced pathological beta oscillations (β, 13-30 Hz) and beta-gamma phase-amplitude coupling (β-γ PAC) in both the M1 and the subthalamic nucleus (STN) of 6-OHDA mice. These physiological recoveries after EGT treatment were accompanied by increased spine density of pyramidal neurons and upregulated expression of glutamate receptors in the M1. Our findings suggest that EGT is a promising natural neuroprotective agent for slowing or preventing PD progression.