Fig. 6: MH can reduce mitochondrial damage in neurons.

A Protective effects of MH on mitochondrial morphology in a ROT-induced PD cell model. a: Mitochondrial morphology of control neurons. b: Mitochondrial morphology in a ROT-induced PD cell model with 200 μM ROT. c: Mitochondrial morphology in a ROT-induced PD cell model with 400 μM ROT. d: Mitochondrial morphology of neuronal cells treated with MH alone. e: Mitochondrial morphology of the PD neuron model induced by 200 μM ROT and treated with MH. f: Mitochondrial morphology of the PD neuron model induced by 400 μM ROT and treated with MH. B–E MH protects mitochondrial function in neurons. Effects of MH pretreatment on ROT-induced oxido-nitrosative stress assessed by B malondialdehyde (MDA) level, C reduced glutathione (GSH) level, and D ATP levels of the hippocampus of the mice in each group. E–H According to the results of mitochondrial dysfunction, we performed western blotting for mitochondrial-related proteins. The western blot (E) was quantified for α-syn (F) and NeuN (G) in the murine hippocampi. The bands were quantified using Sigma Gel software, and the differences are represented by a histogram. GAPDH was used as a loading control. The results showed that both MH and SP could restore the abnormal expression of α-syn (F), NeuN (G), and VDAC (H). The western blot (I) was quantified for TH (J) and HSP60 (K) in the substantia nigra. The bands were quantified using Sigma Gel software, and the differences are represented by a histogram. GAPDH was used as a loading control. The results showed that both MH and SP could restore the abnormal expression of TH (J) and HSP60 (K). All values are expressed as mean ± SEM. All experiments were repeated more than three times individually. Scale bar = 500 μm in 100×. ^*P < 0.05, ^**P < 0.01, and ^***P < 0.001.