Sulforaphane ameliorate Arsenic induced cardiotoxicity in rats: Role of PI3k/Akt mediated Nrf2 signaling pathway.

Arsenic (As) toxicity can generate reactive free radicals, which play an important role in the evolution of cardiomyopathy. The aim of this research is to see if sulforaphane (SFN) protects against As-induced heart damage, oxidative stress, and mitochondrial complex dysfunction via the PI3K/Akt/Nrf2 signaling pathway. The rats were placed into four groups, each with eight rats.

Emerging promise of sulforaphane-mediated Nrf2 signaling cascade against neurological disorders.

Neurological disorders represent a great challenge and are the leading cause of death and disability globally. Although numerous complicated mechanisms are involved in the progressions of chronic and acute neurodegenerative disorders, most of the diseases share mutual pathogenic features such as oxidative stress, mitochondrial dysfunction, neuroinflammation, protein misfolding, excitotoxicity, and neuronal damage, all of these are the common targets of nuclear factor erythroid 2 related factor 2 (Nrf2) signaling cascade. No cure has yet been discovered to tackle these disorders, so, intervention approaches targeting phytochemicals have been recommended as an alternative form of treatment.

Cholinesterase Inhibitors for Alzheimer's Disease: Multitargeting Strategy Based on Anti-Alzheimer's Drugs Repositioning.

In the brain, acetylcholine (ACh) is regarded as one of the major neurotransmitters. During the advancement of Alzheimer's disease (AD) cholinergic deficits occur and this can lead to extensive cognitive dysfunction and decline. Acetylcholinesterase (AChE) remains a highly feasible target for the symptomatic improvement of AD.

Sulforaphane Potentially Ameliorates Arsenic Induced Hepatotoxicity in Albino Wistar Rats: Implication of PI3K/Akt/Nrf2 Signaling Pathway.

Background/aims: Agriculture and industrial expansion in recent years have resulted in the undue discharge of arsenic into the environment, building arsenic toxicity a major worldwide anxiety. Oxidative stress is considered as the most conspicuous effect of arsenic toxicity. The current study was designed to evaluate the protective ability of sulforaphane (SFN) against arsenic (As) induced hepatotoxicity by activation of PI3K induced Akt and Nrf2 mediated signaling pathway.

Sulforaphane potentially attenuates arsenic-induced nephrotoxicity via the PI3K/Akt/Nrf2 pathway in albino Wistar rats.

Oxidative stress plays a significant role in the pathophysiology of numerous kidney diseases, generally mediated by reactive oxygen species (ROS). Arsenic (Ar) is known to exert its toxicity through the generation of ROS and inflammation. The current study investigates the protective effects of sulforaphane (SFN) against arsenic-induced renal damage via PI3K/Akt-mediated Nrf2 pathway signaling.

Epigallocatechin gallate potentially abrogates fluoride induced lung oxidative stress, inflammation via Nrf2/Keap1 signaling pathway in rats: An in-vivo and in-silico study.

Background: Since this Nrf2-dependent cellular defense response is able to protect multi-organs, including cancer, neurodegenerative diseases, cardiovascular diseases, inflammation and chronic lung injury. The antioxidant and anti-inflammatory potential of Epigallocatechin gallate (EGCG) and Nrf2/Keap1 signaling mechanisms in pulmonary toxicity have not been clarified. In the present study, we demonstrated that protective efficacy of EGCG against fluoride (Fl) induced oxidative stress mediated lung injury in rats.

Epigallocatechin gallate effectively ameliorates fluoride-induced oxidative stress and DNA damage in the liver of rats.

Environmental exposure to sodium fluoride (NaF) compounds is a worldwide health concern. Epigallocatechin gallate (EGCG) is a green tea catechin found in a variety of green tea preparations. The intention of this study was to investigate the hepatoprotective role of EGCG in NaF-intoxicated rats.