Published online 2022 Sep 16, I realize it is a rat study, but it is sinomenine is used in Traditional Chinese Medicine.
Pharmacological effects of sinomenine in Parkinson’s disease
PD is a common neurodegenerative disorder characterized by progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta and subsequent depletion of an important neurotransmitter in the striatum that can negatively control motor skills—dopamine (Nemade et al., 2021). Numerous therapeutic methods are available in the clinic, including drug and non-drug treatments, to treat PD. However, considering the low efficacy of treatment and severe side effects, the development of new drugs is always a hot topic for PD research. Administration of sinomenine (i.p., 20 mg/kg, 5 days before treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and for another 4 days) can suppress the MPTP-induced decline in rotarod time, pounds for grip strength, and forepaw stride length in mice, which was accompanied by an increase in tyrosine hydroxylase (TH)-positive cells in the substantia nigra pars compacta (Bao et al., 2022) (Table 2), suggesting that sinomenine administration improves motor skills in mice with PD by promoting the survival of dopaminergic neurons.
Autophagy is a general biological process that mediates the pathogenesis of PD (Sepúlveda et al., 2022). Promoting autophagy is considered a potential strategy for the treatment of PD. Administration of sinomenine can suppress the MPTP-induced decrease in Beclin-1 and LC3-II/LC3-I ratio, as well as the MPTP-induced increase in p62 in the substantia nigra pars compacta of the mouse brain, by inhibiting the protein kinase B (Akt)-mammalian target of rapamycin (mTOR) signaling (Figure 4; Table 2) (Bao et al., 2022), suggesting that triggering autophagy may mediate the action of sinomenine against PD. This hypothesis is supported by the finding that MHY1485, a specific activator of the Akt-mTOR signaling pathway that affects autophagy, further impairs the motor abilities of PD mice and attenuates the beneficial effect of sinomenine on the motor abilities of PD mice by promoting the loss of dopaminergic neurons (Bao et al., 2022).
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FIGURE 4
Effects and mechanisms of sinomenine in pathological conditions resembling PD. Sinomenine can inhibit MPTP-induced dephosphorylation of Akt and mTOR, thereby promoting the process of autophagy by increasing the expression of Beclin-1, increasing the LC3-II/LC3-I ratio, and reducing the accumulation of p62 Bao et al. (2022). Sinomenine may also suppress neuroinflammation triggered by MPP+ or LPS, thereby increasing dopamine uptake Qian et al. (2007).
Another mechanism for the anti-PD effect of sinomenine may be related to the inhibition of neuroinflammation, because pre-incubation with sinomenine (10−6, 10−5, 10−14, 10−13 M) can simultaneously prevent the LPS-induced decrease in the ability of midbrain neuron-enriched cultures to take up dopamine and the LPS-induced decrease in TH-positive neurons in midbrain neuron-enriched cultures (Figure 4; Table 2) (Qian et al., 2007). Mechanistic studies showed that the neuroprotective effect of sinomenine in the above model may be highly related to the attenuating effect of sinomenine on the LPS-induced production of TNF-α, prostaglandin E2 (PGE2), and NO, as well as on the expression of iNOS in rat microglia-enriched cultures (Figure 4; Table 2) (Qian et al., 2007). This hypothesis is also supported by the finding that incubation with sinomenine prevented the MPP+-induced decrease in dopamine uptake in primary mesencephalic neuron-glia cultures by microglia: Sinomenine showed no effect on the toxic effects of 1-methyl-4-phenylpyridiniumion (MPP+) in primary mesencephalic neuron cultures, which was restored when the neuron-enriched cultures were reconstituted with purified microglia but not astrocytes (Qian et al., 2007) (Table 2). Thus, it is possible that sinomenine does not directly protect neurons from MPP+-mediated toxicity, but that targeting microglia is a crucial process. However, it is worth noting that although microglia are known to mediate the pathogenesis of PD through neuroinflammation, sinomenine did not suppress MPP+-induced production of TNF-α and NO in the presence of microglia, but suppressed MPP+-induced production of superoxide in rat mesencephalic neuron-glia cultures, suggesting that inhibition of superoxide-associated oxidative stress, but not neuroinflammation, may mediate the anti-neurotoxic effect of sinomenine (Qian et al., 2007).
I think the best way to incorporate TCM is to see a TCM practicioner.
-Syd
Mitochondrial uncoupling ; can this help PD, appears maybe 
Parkinson's disease is an autoimmune disease: An emerging viewpoint
