myricitrin and Parkinson-Disease

In humans, oxidative stress is thought to be involved in the development of Parkinson's disease, Alzheimer's disease, atherosclerosis, heart failure, myocardial infarction and depression. Myricitrin, a botanical flavone, is abundantly distributed in the root bark of Myrica cerifera, Myrica esculenta, Ampelopsis grossedentata, Nymphaea lotus, Chrysobalanus icaco, and other plants. Considering the abundance of its natural sources, myricitrin is relatively easy to extract and purify. Myricitrin reportedly possesses effective anti-oxidative, anti-inflammatory, and anti-nociceptive activities, and can protect a variety of cells from in vitro and in vivo injuries. Therefore, our current review summarizes the research progress of myricitrin in cardiovascular diseases, nerve injury and anti-inflammatory, and provides new ideas for the development of myricitrin.

Topics: Alzheimer Disease; Animals; Anti-Inflammatory Agents; Cardiovascular Diseases; Flavonoids; Humans; Inflammation; Myrica; Osteoporosis; Oxidative Stress; Parkinson Disease; Phytotherapy

Parkinson's disease (PD) is characterized by the progressive degeneration of dopaminergic (DA) neurons in the substantia nigra pars compacta and decreases in striatal dopamine levels. These changes led to several clinical symptoms: rigidity, resting tremor, and bradykinesia. Although the cause of PD remains unclear, it is widely accepted that oxidative stress, neuroinflammation, mitochondrial dysfunction, and insufficient support of neurotrophic factors are involved in the pathophysiology of the disease. However, novel regimens to prevent neurodegeneration and restore the degenerated nigrostriatal DA system are still required. In recent years, there has been a growing interest in naturally occurring phytochemicals, which are believed to reduce the risk of neurodegenerative diseases. This review provides an overview of the scientific literature concerning the preventive and protective roles of flavonoids, one of the largest families of phytochemicals, against PD. In addition to providing antioxidant and anti-inflammatory effects, flavonoids exhibit a neuroprotective effect by activating antiapoptotic pathways that target mitochondrial dysfunction and induce neurotrophic factors. This review suggests that flavonoids may be promising natural products for the prevention of PD and could potentially be utilized as therapeutic compounds against PD, even though there was no report showing that the treatment with flavonoids could restore the aberrant phenotypes of patients with PD.

Topics: Animals; Anthocyanins; Antioxidants; Antiparkinson Agents; Catechin; Cell Line; Corpus Striatum; Disease Models, Animal; Dopamine; Flavanones; Flavones; Flavonoids; Flavonols; Humans; Isoflavones; Kaempferols; Neuroprotective Agents; Oxidative Stress; Parkinson Disease

Flavonoids exhibit several biological activities including inhibition of Monoamine oxidase (MAO), an enzyme that metabolizes several neurotransmitters. Thus, MAO inhibitors are well included in traditional therapeutic practices to fine-tune neuromotor behavior. This study aims to isolate flavonoids from a less explored plant of northeast India, named Indian olive (

Topics: Animals; Brain; Disease Models, Animal; Dopamine; Elaeocarpaceae; Flavonoids; Mice; Monoamine Oxidase; Monoamine Oxidase Inhibitors; Olea; Parkinson Disease

Parkinson's disease (PD) is a chronic and progressive movement disorder, resulting from the degeneration of the nigrostriatal dopaminergic (DA) pathway. The cause of DA neuronal loss in PD is still unclear; however, accumulating evidence suggests that treatment with certain flavonoids can induce neuroprotective properties, such as activation of mammalian target of rapamycin complex 1 (mTORC1) and anti-inflammatory activities in animal models of PD. The bioflavonoid myricitrin is well known for its anti-inflammatory and antioxidant properties. However, it is unclear whether systemic treatment with myricitrin can protect neurons against neurotoxin-induced DA degeneration in vivo via the preservation of tyrosine hydroxylase (TH) activity and the induction of mTORC1 activation. Our results found no significant neuroprotective effect of 30 mg/kg myricitrin on 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in the substantia nigra (SN) of mice. However, myricitrin treatment with 60 mg/kg protected DA neurons against 6-OHDA-induced neurotoxicity. Moreover, myricitrin treatment preserved TH enzyme activity and mTORC1 activation in nigral DA neurons in the SN of 6-OHDA-treated mice, and its treatment suppressed an increase in tumor necrosis factor-α expression in activated microglia. These results suggest that myricitrin may have neuroprotective properties linked to mTORC1 activation, preservation of TH enzyme activity, and anti-neuroinflammation for preventing DA neuronal degeneration in vivo.

Topics: Animals; Brain; Dopamine; Dopaminergic Neurons; Flavonoids; Humans; Mice; Mice, Inbred C57BL; Neuroprotective Agents; Oxidopamine; Parkinson Disease; Substantia Nigra; Tyrosine 3-Monooxygenase