I started using cacao powder years ago. Having this proven in rats is good enough for me since we will never get human testing done while I'm alive.
Cacao powder supplementation attenuates oxidative stress, cholinergic impairment, and apoptosis in galactose induced aging rat brain
Scientific Reports volume 11, Article number: 17914 (2021)
Abstract
Aging, a critical risk factor of several diseases, including neurodegenerative disorders, affects an ever-growing number of people. Cacao supplementation has been suggested to improve age-related neuronal deficits. Therefore, this study investigated the protective effects of raw cacao powder on oxidative stress-induced aging. Male Sprague–Dawley rats were divided into 4 groups: Control (C), d-galactose-induced aging (G), d-galactose injection with 10% (LC), and 16% (HC) cacao powder mixed diet. d-galactose (300 mg/3 mL/kg) was intraperitoneally injected into all but the control group for 12 weeks. Cacao supplemented diets were provided for 8 weeks. The levels of serum Malondialdehyde (MDA), Advanced Glycation End-products (AGEs), brain and liver MDA, the indicators of the d-galactose induced oxidative stress were significantly decreased in LC and HC but increased in G. The Acetylcholinesterase (AChE) activity of brain showed that the cholinergic impairment was significantly lower in LC, and HC than G. Furthermore, the expression levels of catalase (CAT), phospho-Akt/Akt, and procaspase-3 were significantly increased in LC and HC. In conclusion, cacao consumption attenuated the effects of oxidative stress, cholinergic impairment and apoptosis, indicating its potential in future clinical studies.
Introduction
Aging is a critical risk factor of neurodegenerative disorders as it is a gradual process inducing dysfunction and degeneration of the nervous or immune system, which results in cognitive impairment1,2. Harman explained that aerobic respiration contributes to free radical production leading to the accumulation of oxidative damage, which may lead to aging and death3. The imbalance of production and removal of reactive oxygen species (ROS) induces oxidative stress4, and excessive ROS or deficient enzymatic antioxidants cause lipid peroxidation, DNA damage, and protein oxidation that may lead to dysfunction of the organism5. Additionally, malondialdehyde (MDA) and advanced glycation end-products (AGEs), which deteriorates with aging, were speculated to lead to all kinds of age-related disorders6. Several studies have reported the effect of apoptosis in aging and age-related disease; however, it is not clear whether aging suppresses or enhances apoptosis in vivo. The phosphatidylinositol 3-kinase (PI3K) and Akt (otherwise known as Protein Kinase B) pathway has been implicated as an anti-apoptotic pathway in many different cellular paradigms. Many studies have suggested that Akt regulates cell death regulation resulting in modulation of the degenerative diseases’ pathogenesis and cancer cells3. PI3K and its downstream Akt are suggested to be the vital enzymes in regulating cell growth, metabolism, and survival modulated by growth factors and neurotransmitters4. Activated PI3K induces the activation of Akt, and previous researches have explained that Akt activation may be therapeutic in neurodegenerative diseases5. Though the mechanism is not clear yet, several studies have investigated the neurodegenerative diseases related to modulation of PI3K/Akt signal dysregulation5,6. In addition, Caspase-3 has been shown to be a major effector of apoptosis in cells activated by oxidative stress and ROS7, and the inhibition of oxidative stress may suppress the apoptotic cell death8. Furthermore, it is known that the free radical scavenging enzymes such as SOD, CAT, and GPx exhibit antioxidative effects against oxidative stress8, and impart protection against aging induced by oxidative stress9,10,11. This could be due to the protective effects of decreasing oxidative stress against cell death, which inhibits the age-related changes in neuronal function, viability, and cognition10.
Many studies have investigated the concrete mechanism of aging; however, they are mutually conclusive. Several studies have reported d-galactose as a source of inducing animal senescence. They have shown increased oxidative stress, inflammatory damage, and apoptosis in the lungs, livers, kidneys, and brains of animals12,13,14,15. Therefore, d-galactose injected animals have been used as aging induced or organ injury models steadily.
The polyphenol-rich foods have gained an increasing research interest because of their potential antioxidative, neuroprotective and cognition enhancing effects16,17,18,19,20,21. Cacao contains a large content of polyphenols, including compounds such as (+)-catechin and (−)-epicatechin, as well as procyanidins (58%) that are effective ROS scavengers21,22. A previous study has shown that an LMN diet (a diet enriched in polyphenols and polyunsaturated fatty acids) composed of cocoa, nuts, vegetable oil rich in unsaponifiable fatty acids, and flours rich in soluble fibers exerts protective effects against neuronal loss caused by aging and delays the Aβ plaque formation23. Similarly, another research conducted with cocoa enriched diets provided evidence that cocoa can induce upregulation of mitogen-activated kinase (MAP) phosphatase MKP, prevent inflammatory responses in trigeminal ganglion neurons, and be an effective treatment of migraine21. (−)-Epicatechin, a flavanol in cacao, has shown preventive effect against stroke through Nrf2 activation and neuroprotective Heme Oxygenase-1(HO-1) increase22.
However, the mechanisms of the protective effects of cacao in aging models are not clear yet. To the best of our knowledge, this is the first study to investigate the protective effects of cacao powder in the d-galactose-induced aging model. The present study observed the d-galactose-induced oxidative stress and protective effects of cacao powder against oxidative stress, cholinergic impairment, and apoptosis.
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