Today, environmental pollution has been found to be one of the causes of various diseases, including brain and nervous system diseases. In particular, neurodegenerative diseases have been found to be caused by hyperactivation of immune system cells such as microglia. Preventive and therapeutic measures are needed to suppress them. Hirudo is known as a traditional herbal medicine, based on its multiple biological activities such as anti-eczema and anti-coagulation. In the present study, the anti-neuroinflammatory potential of hirudo extract was investigated in lipopolysccharide (LPS)-stimulated BV2 microglial cells and in mice. Hirudo extract significantly inhibited LPS-stimulated nitric oxide (NO) production and cytokine (IL-1Ra, KC, MCP-5, and RANTES) expression in a dose-dependent manner without causing cytotoxicity. Pretreatment with hirudo extract suppressed LPS-induced NF-κB p65 nuclear translocation. Moreover, hirudo extract reduced LPS-stimulated microglial acitivation and improved memory impairments. The results demonstrated that hirudo extract exerts anti-neuroinflammation activities, partly through inhibition of the NF-κB signaling pathway. These findings suggest that hirudo extract might have therapeutic potential with respect to neuroinflammation and neurodegenerative diseases.

Under constant environmental pollution, the incidence of Atopic Dermatitis (AD) caused by air pollutants and allergens has increased. AD is an allergy inflammatory skin disease characterized by pruritus, eczema, and skin dryness. In herbal medicine, Anemarrhena asphodeloides (Anemarrhenae Rhizoma; AR) has been utilized to treat Alzheimer’s disease, osteoporosis, hypertension, and inflammation. The purpose of study evaluated the effect of AR in a mouse model of 2,4-dinitrochlorobenzene (DNCB)-induced AD-like skin lesions. After acclimatization for 5 days, the mice (6-week-old, male Balb/c) were divided into five groups (n=6/group): NC (normal control), DNCB (control), Dex (5 mg·kg-1, p.o.), AR100 (100 mg·kg-1, p.o.), and AR300 (300 mg·kg-1, p.o.). On days 1 and 3, 1% DNCB was applied to the skin and ears. After 4 days, 0.5% DNCB was applied once every 2 days for 2 weeks. Then, skin and ears eczema area and severity index (EASI); skin nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and prostaglandin E2 (PGE2) levels; and plasma immunoglobulin E (IgE) levels were examined. The AR groups showed lower EASI, skin and ear thickness, mast cell count, and IgE levels than the control groups. Moreover, AR reduced iNOS, COX-2, and PGE2 levels. Therefore, AR possesses anti-inflammatory properties and can improve skin damage, indicating its therapeutic potential against AD.

Parkinson’s Disease (PD) is a chronic neurodegenerative disorder caused by the progressive loss of dopaminergic neurons, leading to decreased dopamine levels in the midbrain. Although the specific etiology of PD is not yet known, oxidative stress, inflammation, and subsequent apoptosis have been proposed to be closely related to PD pathophysiology. Cera Flava (CF) is a natural extract obtained from beehives and is isolated through the heating, compression, filtration, and purification of beehives. CF has been used in traditional medicines for its various clinical and pharmacological effects. However, its effects on neurodegenerative diseases are unknown. Therefore, we investigated the effects of CF against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD in mice and explored the underlying mechanism of action. In MPTP-induced PC12 cells, CF protected NADH dehydrogenase activity and inhibited lactate dehydrogenase. In the mouse model, CF promoted recovery from movement impairments, prevented dopamine depletion, and protected against MPTP-induced dopaminergic neuronal degradation. Moreover, CF downregulated glial and microglial activation. Taken together, our results suggest that CF improves behavioral impairments and protects against dopamine depletion in MPTP-induced toxicity by inhibiting glial and microglial activation.