Leonurine ameliorates D-galactose-induced aging in mice through activation of the Nrf2 signalling pathway

Abstract

Aging is a complex physiological phenomenon associated with oxidative stress damage. The objective of this study was to investigate the potential effects of leonurine on D-galactose-induced aging in mice and its possible mechanisms. In this study, we first tested the antioxidant activity of leonurine in vitro. A subcutaneous injection of D-galactose in mice for 8 weeks was used to establish the aging model to evaluate the protective effects of leonurine. The results showed that treatment with 150 mg·kg-1 leonurine could improve the mental condition, organic index, and behavioural impairment; significantly increase the activities of antioxidative enzymes including SOD, CAT, and T-AOC; and ameliorate the advanced glycation end product (AGE) level and histopathological injury. Furthermore, the Western blotting data revealed that leonurine supplementation noticeably modulated the suppression of the Nrf2 pathway and upregulated the downstream expression of HO-1 and NOQ1 in aging mice. Additionally, leonurine treatment activated Nrf2 nuclear translocation in both aging mice and normal young mice, and the expression levels of Nrf2 in normal young mice was higher than those in naturally aging mice. In conclusion, our findings suggest that leonurine is a promising agent for attenuating the aging process, and the underlying molecular mechanisms depend on activating the Nrf2 pathway.

Alginate Oligosaccharide Ameliorates D-Galactose-Induced Kidney Aging in Mice through Activation of the Nrf2 Signaling Pathway

“…Our further investigations indicated that AOS supplementation potently activated the Nrf2 signaling pathway by increasing the Nrf2 transcription level and facilitated the expression of the Nrf2 downstream target genes HO-1 and NQO1 in aging model mice. These results are in line with those of previous studies [ 7 , 47 ].…”

“…The antioxidant defense system has been proven to play a major role in senescence by regulating intracellular redox balance [ 6 ]. Therefore, resistance to oxidative stress may be a promising therapeutic strategy for delaying the kidney aging process [ 7 ].…”

The therapeutic value of XL388 in human glioma cells

“…Inhibition of Nrf2 signaling could lead to ROS production and oxidative injury [ 21 , 33 , 34 ]. By measuring CellROX fluorescence [ 35 , 36 ], we show that XL388 induced significant ROS production in A172 cells ( Figure 4D ).…”

The Protective Effect of Adiponectin-Transfected Endothelial Progenitor Cells on Cognitive Function in D-Galactose-Induced Aging Rats

“…In D-gal-induced aging rat model, the excessive and long-term injection of D-gal can lead to the overproduction of AGEs and ROS, which may result strong oxidative stress and chronic inflammation that accelerates aging in rats [9][10][11][12][13]. Chronic, aseptic, and low-degree inflammation was considered a sign of the aging process [2].…”

“…Excessive long-term D-gal intake can lead to the overproduction of advanced glycosylation end-products (AGEs) and reactive oxygen species (ROS) [5], which may contribute to chronic inflammation and oxidative stress [6]. Many studies have shown that chronic inflammation and oxidative stress would result in mitochondrial, neurological function damage, and even cognitive decline [7][8][9][10][11][12]. The model of accelerated aging with long-term injection of D-gal has been widely used in antiaging studies, due to the increase of chronic inflammation, decline of cognition, and biochemical indexes that are similar with natural aging in animals [5][6][7][8][9][10][11][12][13].…”