RESUMEN
Parkinson's disease (PD) is a prevalent neurodegenerative disease marked by dopaminergic neuronal loss and misfolded alpha-synuclein (α-syn) accumulation, which results in both motor and cognitive symptoms. Its occurrence grows with age, with a larger prevalence among males. Despite substantial study, effective medicines to reduce or stop the progression of diseases remain elusive. Interest has grown in examining dietary components, such as caffeine present in coffee, for potential medicinal effects. Epidemiological studies imply a lower incidence of PD with coffee drinking, attributable to caffeine's neuroprotective abilities. Beyond caffeine, coffee constituent like chlorogenic acid and cafestol have anti-Parkinsonian benefits. Moreover, coffee use has been related with variations in gut microbiota composition, which may reduce intestinal inflammation and prevent protein misfolding in enteric nerves, perhaps through the microbiota-gut-brain axis. This review gives a summary of the neuroprotective effects of coffee, investigating both its motor and non-motor advantages in individuals with PD as well as in experimental models of PD. We reviewed some bioactive constituents of coffee, their respective interactions with misfolded α-syn accumulation, and its emerging mechanisms associated to the gut microbiome.
Asunto(s)
Café , Microbioma Gastrointestinal , Enfermedad de Parkinson , Humanos , Enfermedad de Parkinson/metabolismo , Animales , Microbioma Gastrointestinal/fisiología , Microbioma Gastrointestinal/efectos de los fármacos , Fármacos Neuroprotectores/farmacología , alfa-Sinucleína/metabolismo , Cafeína/farmacologíaRESUMEN
This study investigated the effects of 6-gingerol-rich fraction of Zingiber officinale (6-GIRIFZO) on mercury chloride (HgCl2)-induced neurotoxicity in Wistar rats. Thirty -five male Wistar rats weighing between (150-200 g) were divided randomly into five groups (n = 7): group 1: control, received 0.5 mL of normal saline, group 2: received HgCl2 (5 mg/kg), group 3: received N-acetylcysteine (NAC) (50 mg/kg) as well as HgCl2 (5 mg/kg), group 4: received 6-GIRIFZO (100 mg/kg) and HgCl2 (5 mg/kg), group 5: had 6-GIRIFZO (200 mg/kg) and HgCl2 (5 mg/kg), consecutively for 14 days. On the day14, the rats were subjected to behavioural tests using a Morris water maze and novel object recognition tests. The rats were then euthanized to obtain brain samples for the determination of biochemical parameters (acetylcholinesterase (AchE), nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione (GSH), tumor necrosis factor- alpha (TNF-α), nuclear factor kappa-B (NF-κB), interleukin-1ß (IL-1ß) and interleukin-6 (IL-6)) using standard methods. The result revealed a significant increase in escape latency and a significant decrease in recognition ratio in the rats that were exposed to HgCl2 only. However, 6-GIRIFZO produced a significant reduction in the escape latency and (p < 0.05) increase in the recognition ratio. Similarly, HgCl2 exposure caused a significant (p < 0.05) decrease in the brain SOD, GPx, CAT, GSH with increased brain levels of MDA, NO, AchE, TNF-α, NF-κB, IL-1ß and IL-6. Similarly to the standard drug, NAC, 6-GIRIFZO (100 and 200 mg/kg) significantly (p < 0.05) increased brain SOD, GPx, CAT, and GSH levels with decreased concentrations of MDA, NO, AchE, TNF-α, NF-κB, IL-1ß and IL-6. Also, pre-treatment with 6-GIRIFZO prevented the HgCl2-induced morphological aberrations in the rats. This study concludes that 6-GIRIFZO prevents HgCl2-induced cognitive deficit via reduction of brain inflammation as well as oxidative stress in rats.
Asunto(s)
Catecoles , Disfunción Cognitiva , Alcoholes Grasos , Mercurio , Zingiber officinale , Ratas , Masculino , Animales , Antioxidantes/farmacología , Antioxidantes/metabolismo , Ratas Wistar , Cloruros , Enfermedades Neuroinflamatorias , Cloruro de Mercurio/toxicidad , Factor de Necrosis Tumoral alfa/metabolismo , FN-kappa B/metabolismo , Interleucina-6 , Acetilcolinesterasa , Estrés Oxidativo , Glutatión/metabolismo , Acetilcisteína/farmacología , Superóxido Dismutasa/metabolismo , Mercurio/farmacologíaRESUMEN
Polycystic ovarian syndrome (PCOS) is an endocrine disorder in women's reproductive age. Currently, the pathophysiology of PCOS is unclear, and the limited treatment options are unsatisfactory. Virgin coconut oil (VCO) is functional food oil associated with pharmacological effects in reproductive disorders. Therefore, we aimed to evaluate whether VCO could enhance clomiphene (CLO) therapy against PCOS in female rats. Rats were randomly divided: (1) Control, (2) PCOS model, (3) PCOS + CLO, (4) PCOS + VCO, and (5) PCOS + CLO + VCO. The PCOS was induced via daily letrozole (1 mg/kg, orally) administration for 21 days. After the PCOS induction, CLO, VCO, and CLO + VCO were administered from days 22 to 36. Serum levels of gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone, estrogen, progesterone, and prolactin were estimated. Polymerase chain reaction gene expression for nuclear factor-erythroid-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), catalase (CAT), glutathione reductase (GSR), LH receptor (LHr), androgen receptor (AR), tumor necrosis factor-alpha (TNF-α), interleukin-1ß (IL-1ß), and caspase-3 were analyzed. The letrozole-induced PCOS caused considerable increases in GnRH, LH, prolactin, estrogen, and testosterone, whereas FSH decreased significantly compared to the control. The gene expression of Nrf2, HO-1, CAT, and GSR were markedly diminished, while IL-1ß, TNF-α, caspase-3, AR, and LHr prominently increased compared to control. Interestingly, the CLO and VCO separately exerted anti-inflammatory and endocrine balance effects. However, VCO-enhanced CLO effect in LH, prolactin and testosterone, Nrf2, HO-1, CAT, GSR, and AR. VCO may synergize with CLO to depress hyperandrogenism and oxidative inflammation in PCOS.