Catalpol, an iridoid glucoside, is widely distributed in many plant families and is primarily obtained from the root of Rehmannia glutinosa Libosch. Rehmannia glutinosa is a plant very commonly used in Chinese and Korean traditional medicine for various disorders, including diabetes mellitus, neuronal disorders, and inflammation. Catalpol has been studied extensively for its biological properties both in vitro and in vivo. This review aims to appraise the biological effects of catalpol and their underlying mechanisms. An extensive literature search was conducted using the keyword “Catalpol” in the public domains of Google scholar, PubMed, and Scifinder. Catalpol exhibits anti-diabetic, cardiovascular protective, neuroprotective, anticancer, hepatoprotective, anti-inflammatory, and anti-oxidant effects in experimental studies. Anti-inflammatory and antioxidant properties are mostly related for its biological effect. However, some specific mechanisms are also elucidated. Elevated serotonin and BDNF level by catalpol significantly protect against depression and neurodegeneration. Catalpol demonstrated an increased mitochondrial biogenesis and activation of PI3K/Akt pathway for insulin sensitizing effect. Further, its cardiovascular protective effect was linked to PI3K/Akt, apelin/APJ and Jak-Stat pathway. Catalpol produced a significant reduction in cell proliferation and an increase in apoptosis in different cancer conditions. Overall, catalpol demonstrated multiple biological effects due to its numerous mechanisms including anti-inflammatory and antioxidant effects.
Background & Objective:
The interlink between diabetes mellitus and neurodegenerative diseases such as Alzheimer’s
disease (AD) and Parkinson’s disease (PD) has been identified by several researchers. Patients with type-2 diabetes mellitus (T2DM)
are found to be affected with cognitive impairments leading to learning and memory deficit, while patients with type-1 diabetes mellitus (T1DM) showed less severe levels of these impairments in the brain. This review aimed to discuss the connection between insulin
with the pathophysiology of neurodegenerative diseases (AD and PD) and the current therapeutic approached mediated through insulin for management of neurodegenerative diseases. An extensive literature search was conducted using keywords “insulin”; “insulin
resistance”; “Alzheimer’s disease”; “Parkinson’s disease” in public domains of Google scholar, PubMed, and ScienceDirect. Selected
articles were used to construct this review. Studies have shown that impaired insulin signaling contributes to the accumulation of
amyloid-β, neurofibrillary tangles, tau proteins and α-synuclein in the brain. Whereas, improvement in insulin signaling slows down
the progression of cognitive decline. Various therapeutic approaches for altering the insulin function in the brain have been researched. Besides intranasal insulin, other therapeutics like PPAR-γ agonists, neurotrophins, stem cell therapy and insulin-like growth
factor-1 is under investigation.
Conclusion:
Research has shown that insulin insensitivity in T2DM leads to neurodegeneration through mechanisms involving a
variety of extracellular, membrane receptor, and intracellular signaling pathway disruptions. Some therapeutics, such as intranasal
administration of insulin and neuroactive substances have shown promise but face problems related to genetic background, accessibility to the brain, and invasiveness of the procedures.
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