Kaempferol, a natural plant-origin flavonoid, exhibits therapeutic anti-inflammatory, antioxidant, anticancer, antidiabetic, and neuroprotective properties. Kaempferol acts within several distinct mechanisms like apoptotic induction in cancer cells, enzymatic inhibition, signalling pathway inhibition, and downregulation in cell viability during the G₂/M phase of cell division. This review summarizes the therapeutic effects of kaempferol against several health ailments. The recent progress on kaempferol obtained from fruits and vegetables as an antioxidant, anti-inflammatory, anticancer, antidiabetic, and neuroprotective agent and its mechanisms of action are also discussed. In addition, kaempferol has been reported to be present in wastes and byproducts from post-fruit and vegetable processing. Thus, a paradigm shift towards valorizing fruits and vegetable industrial wastes/byproducts to obtain bioactive kaempferol can support the circular economy pillar for generating wealth from waste and for finding a sustainable alternative source.

Objective: To explore the combinatorial effect of epigallocatechin-3-gallate (EGCG) and calorie restriction on activation of nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor involved in the antioxidant defense system of aged rats. Methods: Aged male Wistar rats were calorie-restricted and treated with EGCG orally for 45 days. The initial body weight of aged rats was recorded, and the final body weight was measured at the end of the experimental period. Serum lipid and lipoprotein status, oxidative stress markers such as free radicals and malondialdehyde levels, and reduced glutathione were assessed. In addition, RT-PCR and Western blotting analyses were performed. Results: Calorie restriction potentiated the effect of EGCG on enhancing antioxidant status, improving the levels of serum lipid and lipoproteins, upregulating Nrf2 and Bcl2, and downregulating Keap1, cullin3, Bax and cytochrome c in aged rats. Conclusions: Calorie restriction can promote EGCG-mediated Nrf2 activation in aged rats. This preliminary finding paves the way for a combinatory approach to replenishing the antioxidant status during aging, thereby reducing the risk for age-associated degenerative diseases.

Objective: To assess the effect of sericin against pentylenetetrazole (PTZ) kindling epilepsy and its associated comorbidities. Methods: Epilepsy was induced with PTZ at the dose of 30 mg/kg i.p. on alternative days for 25 days in rats. Sericin was administered orally at the doses of 250, 500, and 1 000 mg/kg for 35 days. The behavioral activities were performed using an elevated plus maze, forced swim test, and Morris water maze test. A PTZ challenge test was conducted on day 32. On day 35, rats were sacrificed to perform oxidative stress, mitochondrial dysfunction, neuroinflammation, neurotransmitters, GABA-T activity, and histopathological analyses. Results: Sericin at 500 and 1 000 mg/kg significantly reduced behavioral changes and neuroinflammatory cytokines, as well as improved oxidative stress, mitochondrial enzyme complex activity, neurotransmitter level, and GABA-T enzymatic activity (P<0.05). Moreover, sericin improved the neuronal survival altered by PTZ kindling in rat hippocampus. Conclusions: Sericin mitigates epilepsy-associated secondary complications possibly by the modulation of mitochondrial enzyme complexes and GABA-T enzymatic activity.

Objective: To investigate the cardioprotective effect of naringenin against isoproterenol (ISO)-induced cardiotoxicity in rats. Methods: Rats were divided into five groups: the normal group, the ISO group (85 mg/kg b.w.); the ISO+naringenin (50 mg/kg b.w.) group, the ISO+naringenin (100 mg/kg b.w.) group and the ISO+propranolol (10 mg/kg b.w.) group. Plasma creatine kinase-MB (CK-MB), cardiac troponin T, lactate dehydrogenase, brain natriuretic peptide (BNP), and IL-10, as well as cardiac transforming growth factor-β1 (TGF-β1), vascular endothelial growth factor (VEGF) and malondialdehyde (MDA) were examined. In addition, NLRP3 and mRNA-208a expressions were evaluated by RT-PCR analysis. Histopathological examination was also performed to assess cardiac damages. Results: Naringenin treatment significantly decreased plasma lactate dehydrogenase, CK-MB, cardiac troponin T, BNP, and IL-10, as well as cardiac TGF-β1, VEGF, and MDA while increasing p-Akt and superoxide dismutase in ISO-administered rats. It also reduced NLRP3 and mRNA-208a gene expression levels. Furthermore, naringenin improved ISO-induced cardiac damage. Conclusions: Naringenin attenuates myocardial dysfunction in ISO-treated rats by decreasing oxidative stress and increasing cardiac endogenous antioxidant system, which may be modulated partly by improvement of NLRP3 and mRNA-208a gene expression.