[Effects of electroacupuncture on the SIRT3/NF-κB /MAPK signaling pathway in the substantia nigra of mice with Parkinson's disease].
[Effects of electroacupuncture on the SIRT3/NF-κB /MAPK signaling pathway in the substantia nigra of mice with Parkinson's disease].
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Wuhan, CN · Author affiliation
College of Acupuncture-moxibustion and Orthopaedics-traumatology, Hubei University of Chinese Medicine, Wuhan 430065, China.Location evidence
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Original abstract
OBJECTIVES: To investigate the effects of electroacupuncture (EA) at "Fengfu" (GV16) and "Taichong" (LR3) on tyrosine hydroxylase (TH), microglia (MG), and the silent information regulator 3(SIRT3)/nuclear factor-kappa B (NF-κB)/mitogen-activated protein kinase (MAPK) signaling pathway-related proteins in the substantia nigra of Parkinson's disease (PD) mice, and to explore the potential mechanisms underlying the therapeutic effects of EA on PD. METHODS: C57BL/6J mice were randomly divided into 4 groups:control group, model group, non-acupoint group, and EA group, with 12 mice in each group. A PD model was established by intraperitoneal injections of MPTP for 7 consecutive days. The EA group received EA at GV16 and LR3. The non-acupoint group underwent needle insertion 3 mm lateral to GV16 and LR3 without electrical stimulation. Treatments were administered for 15 min per session, once daily for 14 days. Motor function was assessed using the pole test and suspension test. Immunohistochemistry was used to detect TH-positive expression in the substantia nigra. Immunofluorescence was employed to quantify activated MG. Western blot was used to measure the protein expression levels of SIRT3, NF-κB p65, and p38 MAPK. ELISA was used to determine the serum levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). RESULTS: Compared with the control group, the model group exhibited a longer total time in the pole test (P<0.01), a lower score in the suspension test (P<0.01), a reduce in mean TH optical density in the substantia nigra (P<0.01), an increase in the number of MG-positive cells (P<0.01), a decrease in SIRT3 protein expression (P<0.01). The protein expression levels of NF-κB p65 and p38 MAPK proteins in the substantia nigra, and the serum levels of TNF-α, and IL-1β were all elevated (P<0.01). Compared with model group and the non-acupoint group, the EA group showed a shortened total time in the pole test (P<0.01), a higher score in the suspension test (P<0.01), an increase in mean TH optical density in the substantia nigra (P<0.01), a decrease in the number of MG-positive cells (P<0.01), an increase in SIRT3 protein expression (P<0.05). The expression levels of NF-κB p65 and p38 MAPK proteins in the substantia nigra, and the serum contents of TNF-α and IL-1β were all decreased (P<0.01). CONCLUSIONS: EA can improve motor dysfunction in PD mice, reduce the loss of dopaminergic neurons, and increase TH expression in the substantia nigra. The underlying mechanism may involve the modulation of the SIRT3/NF-κB/MAPK signaling pathway to suppress neuroinflammation.