Phikud navakot extract acts as an ER stress inhibitor to ameliorate ER stress and neuroinflammation.

The prevalence of neurological disorders (NDs) such as Alzheimer's disease (AD) is increasing globally, and the lack of effective pharmacological interventions presents a significant health risk. Multiple mechanisms including the activation of oxidative stress, amyloid pathway, ER stress, and neuroinflammation have been implicated in AD; therefore, multi-targeted agents against these mechanisms may be preferable to single-target agents. Phikud Navakot (PN), a Thai traditional medicine combining nine herbs, has been shown to reduce oxidative stress and neuroinflammation of neuronal and microglia cells and the coculture between them, indicating the promising role of PN extract as anti-AD.

Extracts Protect Neural Stem Cells from Amyloid Peptide-Mediated Inflammation in Co-Culture Model with Microglia.

The existence of neuroinflammation and oxidative stress surrounding amyloid beta (Aβ) plaques, a hallmark of Alzheimer's disease (AD), has been demonstrated and may result in the activation of neuronal death and inhibition of neurogenesis. Therefore, dysregulation of neuroinflammation and oxidative stress is one possible therapeutic target for AD. Wall.

Antidiabetic effects of supplementation on biochemical parameters, inflammatory responses, and oxidative stress in canine diabetes.

Diabetes mellitus is a common endocrine disorder that causes hyperglycemia in dogs. Persistent hyperglycemia can induce inflammation and oxidative stress. This study aimed to investigate the effects of (Burm.

Phikud Navakot extract attenuates lipopolysaccharide-induced inflammatory responses through inhibition of ERK1/2 phosphorylation in a coculture system of microglia and neuronal cells.

Ethnopharmacological Relevance: Phikud Navakot (PN), a mixture of nine herbal plants, is an ancient Thai traditional medicine used for relieving circulatory disorders and dizziness. PN has also shown anti-inflammatory effects in rats with acute myocardial infarction. Moreover, phytochemical-inhibiting neuroinflammation, including gallic acid, vanillic acid, ferulic acid, and rutin were detected in PN extract; however, the anti-neuroinflammatory activity of PN extract and its components in a coculture system of microglia and neuronal cells is limited.

Corticosterone potentiates ochratoxin A-induced microglial activation.

Microglial activation in the central nervous system (CNS) has been associated with brain damage and neurodegenerative disorders. Ochratoxin A (OTA) is a mycotoxin that occurs naturally in food and feed and has been associated with neurotoxicity, while corticosteroids are CNS' physiological function modulators. This study examined how OTA affected microglia activation and how corticosteroids influenced microglial neuroinflammation.