The human gut harbors microbial ecology that is in a symbiotic relationship with its host and has a vital function in keeping host homeostasis. Inimical alterations in the composition of gut microbiota, known as gut dysbiosis, have been associated with cardiometabolic diseases. Studies have revealed the variation in gut microbiota composition in healthy individuals as compared to the composition of those with cardiometabolic diseases. Perturbation of host–microbial interaction attenuates physiological processes and may incite several cardiometabolic disease pathways. This imbalance contributes to cardiometabolic diseases via metabolism-independent and metabolite-dependent pathways. The aim of this review was to elucidate studies that have demonstrated the complex relationship between the intestinal microbiota as well as their metabolites and the development/progression of cardiometabolic diseases. Furthermore, we systematically itemized the potential therapeutic approaches for cardiometabolic diseases that target gut microbiota and/or their metabolites by following the pathophysiological pathways of disease development. These approaches include the use of diet, prebiotics, and probiotics. With the exposition of the link between gut microbiota and cardiometabolic diseases, the human gut microbiota therefore becomes a potential therapeutic target in the development of novel cardiometabolic agents.
Paraquat (PQ) is a dopaminergic neurotoxin and a well-known pneumotoxicant that exerts its toxic effect via oxidative stress-mediated cellular injuries. This study investigated the protective effects of Tualang honey against PQ-induced toxicity in the midbrain and lungs of rats. The rats were orally treated with distilled water (2 mL/kg/day), Tualang honey (1.0 g/kg/day), or ubiquinol (0.2 g/kg/day) throughout the experimental period. Two weeks after the respective treatments, the rats were injected intraperitoneally with saline (1 mL/kg/week) or PQ (10 mg/kg/week) once per week for four consecutive weeks. After four weekly exposures to PQ, the glutathione peroxidase activity and the number of tyrosine-hydroxylase immunopositive neurons in the midbrain were significantly decreased in animals from group PQ (p < 0.05). The lungs of animals from group PQ showed significantly decreased activity of superoxide dismutase and glutathione-S-transferase. Treatment with Tualang honey ameliorated the toxic effects observed in the midbrain and lungs. The beneficial effects of Tualang honey were comparable to those of ubiquinol, which was used as a positive control. These findings suggest that treatment with Tualang honey may protect against PQ-induced toxicity in the rat midbrain and lung.
Objective: The objective of this research was to investigate the possible protective effect of Tualang honey (TH) in acute paraquat (PQ) toxicity in rats.Methods: A total of 48 male Sprague-Dawley rats aged eight weeks old were used. Oral PQ and TH were administered at 225 mg/kg and 0.2 g/kg, respectively. The effects of single and multiple TH treatmentson PQ-intoxicated rats were then investigated. Single TH treatment groups received TH at 0.5 (PQ+TH0.5h), 2 (PQ+TH2h) or 6 (PQ+TH6h) hours following PQ administration. Multiple TH treatment groups received TH at 0.5, 2 and 6 h (PQ+THtrp) or further daily treatment for the following six days (PQ+TH7d) after PQ administration (n=6 per group). The survival time of the rat was recorded until day 28 before sacrifice, which was followed by a histological examination.Results: Treatment with TH did not improve the survival rate of PQ-intoxicated rats. However, the median survival time of rats that received multiple TH treatments was significantly longer compared to that of the PQ+TH6h group. TH treatment was found to improve the histological outcomes of PQ-intoxicated rats, particularly in the lungs. Conclusion:Our findings suggest the potential role of honey in delaying the toxic effects of PQ.
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