Qiangji Decoction Alleviates Neurodegenerative Changes and Hippocampal Neuron Apoptosis Induced by D-Galactose via Regulating AMPK/SIRT1/NF-κB Signaling Pathway

Abstract

Qiangji Decoction (QJD), a classic formula, has been widely used to treat brain aging–related neurodegenerative diseases. However, the mechanisms underlying QJD’s improvement in cognitive impairment of neurodegenerative diseases remain unclear. In this study, we employed D-galactose to establish the model of brain aging by long-term D-galactose subcutaneous injection. Next, we investigated QJD’s effect on cognitive function of the model of brain aging and the mechanisms that QJD suppressing neuroinflammation as well as improving neurodegenerative changes and hippocampal neuron apoptosis. The mice of brain aging were treated with three different dosages of QJD (12.48, 24.96, and 49.92 g/kg/d, respectively) for 4 weeks. Morris water maze was used to determine the learning and memory ability of the mice. HE staining and FJB staining were used to detect the neurodegenerative changes. Nissl staining and TUNEL staining were employed to detect the hippocampal neuron apoptosis. The contents of TNF-α, IL-1β, and IL-6 in the hippocampus were detected by using ELISA. Meanwhile, we employed immunofluorescence staining to examine the levels of GFAP and IBA1 in the hippocampus. Besides, the protein expression levels of Bcl-2, Bax, caspase-3, cleaved caspase-3, AMPKα, p-AMPKα-Thr172, SIRT1, IκBα, NF-κB p65, p-IκBα-Ser32, and p-NF-κB p65-Ser536 in the hippocampus of different groups were detected by Western blot (WB). Our findings showed that the QJD-treated groups, especially the M-QJD group, mitigated learning and memory impairments of the model of brain aging as well as the improvement of neurodegenerative changes and hippocampal neuron apoptosis. Moreover, the M-QJD markedly attenuated the neuroinflammation by regulating the AMPK/SIRT1/NF-κB signaling pathway. Taken together, QJD alleviated neurodegenerative changes and hippocampal neuron apoptosis in the model of brain aging via regulating the AMPK/SIRT1/NF-κB signaling pathway.

Geraniol attenuates oxidative stress and neuroinflammation-mediated cognitive impairment in D galactose-induced mouse aging model

“…D-gal induced aging was tied to hippocampal apoptosis, according to accumulating evidence [ 53 , 54 ]. We used Western blot to examine whether, GNL supplementation inhibited apoptosis.…”

Artesunate Combined With Metformin Ameliorate on Diabetes-Induced Xerostomia by Mitigating Superior Salivatory Nucleus and Salivary Glands Injury in Type 2 Diabetic Rats via the PI3K/AKT Pathway

“…However, increased TUNEL + cells in the Dia group were inhibited by treatments with ART or Met alone and ART/Met combination, among of which ART/Met combination exhibited the best suppressive effect in TUNEL + cells increase ( p < 0.01; Figure 8A ). Furthermore, expression levels of typical apoptosis-related markers (Bax, Caspase3, and Bcl-2) ( He et al, 2021 ), were evaluated using Western blot. The results showed that the expression levels of Bax and Caspase3 protein in the untreated diabetic group were upregulated ( p < 0.01; Figure 8B ), while expression level of Bcl-2 protein was downregulated compared to the normal control group ( p < 0.01; Figure 8B ).…”

D-mannose alleviates chronic periodontitis in rats by regulating the functions of neutrophils

“…It has been unraveled that glycolysis can promote in ammation in endothelial cells [39]. The blockade of glycolysis suppressed the LPS-induced macrophage pyroptosis, resulting in an attenuation of the in ammatory response and bone resorption in periodontitis [40]. It was found that HK2-mediated glycolysis promoted in ammatory responses in human gingival broblasts in gingival tissues [41].…”