Salvianolic Acid B improves cognitive impairment by inhibiting neuroinflammation and decreasing Aβ level in <i>Porphyromonas gingivalis</i>-infected mice

Liu, Jianwei; Wang, Yiling; Jing, Guo; Sun, Jinyan; Sun, Qiang

doi:10.18632/aging.103306

Cited by 25 publications

(21 citation statements)

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“…The bidirectional interaction between Aβ deposition and neuroinflammation resulted in the apoptosis of neurocytes and then impaired cognitive function in the Pg group. It is reported that inhibition of Pg-induced neuroinflammation can decrease the deposition of Aβ ( Dominy et al., 2019 ; Liu et al., 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Porphyromonas gingivalis-Induced Cognitive Impairment Is Associated With Gut Dysbiosis, Neuroinflammation, and Glymphatic Dysfunction

Xiao

Lin³

et al. 2021

Front. Cell. Infect. Microbiol.

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BackgroundPeriodontal pathogen and gut microbiota are closely associated with the pathogenesis of Alzheimer’s disease (AD). Porphyromonas gingivalis (Pg), the keystone periodontal pathogen, can induce cognitive impairment. The gut has a connection and communication with the brain, which is an important aspect of the gut–brain axis (GBA). In the present study, we investigate whether Pg induces cognitive impairment through disturbing the GBA.MethodsIn this study, Pg was orally administered to mice, three times a week for 1 month. The effects of Pg administration on the gut and brain were evaluated through behaviors, gut microbiota, immune cells, glymphatic pathway clearance, and neuroinflammation.ResultsPg induced cognitive impairment and dysbiosis of gut microbiota. The α-diversity parameters did not show significant change after Pg administration. The β-diversity demonstrated that the gut microbiota compositions were different between the Pg-administered and control groups. At the species level, the Pg group displayed a lower abundance of Parabacteroides gordonii and Ruminococcus callidus than the control group, but a higher abundance of Mucispirillum schaedleri. The proportions of lymphocytes in the periphery and myeloid cells infiltrating the brain were increased in Pg-treated animals. In addition, the solute clearance efficiency of the glymphatic system decreased. Neurons in the hippocampus and cortex regions were reduced in mice treated with Pg. Microglia, astrocytes, and apoptotic cells were increased. Furthermore, amyloid plaque appeared in the hippocampus and cortex regions in Pg-treated mice.ConclusionsThese findings indicate that Pg may play an important role in gut dysbiosis, neuroinflammation, and glymphatic system impairment, which may in turn lead to cognitive impairment.

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Section: Discussionmentioning

confidence: 99%

Porphyromonas gingivalis-Induced Cognitive Impairment Is Associated With Gut Dysbiosis, Neuroinflammation, and Glymphatic Dysfunction

Xiao

Lin³

et al. 2021

Front. Cell. Infect. Microbiol.

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“…Histologically, chronic P gingivalis or P gingivalis LPS administration increased the number of activated microglial cells and astrocytes in the cortex 148,153 and in the hippocampus 143,145,150,152,154 as an indicator of the local inflammation. Pro‐inflammatory mediators, like IL‐1β, IL‐6, TNFα, INF‐γ, were elevated compared to controls on mRNA and protein level 143,144,146‐150,152‐154 …”

Section: Porphyromonas Gingivalis – Animal and In Vitro‐studiesmentioning

confidence: 99%

“…Proinflammatory mediators, like IL-1β, IL-6, TNFα, INFγ, were elevated compared to controls on mRNA and protein level. 143,144,[146][147][148][149][150][152][153][154] In terms of the β amyloid deposition, precursor proteins (APP)…”

Section: Animal Studiesmentioning

confidence: 99%

Periodontal microorganisms and Alzheimer disease – A causative relationship?

Jungbauer

Stähli

Zhu

et al. 2022

Periodontology 2000

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In the initiation or exacerbation of Alzheimer disease, the dissemination of oral microorganisms into the brain tissue or the low‐level systemic inflammation have been speculated to play a role. However, the impact of oral microorganisms, such as Porphyromonas gingivalis, on the pathogenesis of Alzheimer disease and the potential causative relationship is still unclear. The present review has critically reviewed the literature by examining the following aspects: (a) the oral microbiome and the immune response in the elderly population, (b) human studies on the association between periodontal and gut microorganisms and Alzheimer disease, (c) animal and in vitro studies on microorganisms and Alzheimer disease, and (d) preventive and therapeutic approaches. Factors contributing to microbial dysbiosis seem to be aging, local inflammation, systemic diseases, wearing of dentures, living in nursing homes and no access to adequate oral hygiene measures. Porphyromonas gingivalis was detectable in post‐mortem brain samples. Microbiome analyses of saliva samples or oral biofilms showed a decreased microbial diversity and a different composition in Alzheimer disease compared to cognitively healthy subjects. Many in‐vitro and animal studies underline the potential of P gingivalis to induce Alzheimer disease‐related alterations. In animal models, recurring applications of P gingivalis or its components increased pro‐inflammatory mediators and β‐amyloid in the brain and deteriorated the animals' cognitive performance. Since periodontitis is the result of a disturbed microbial homoeostasis, an effect of periodontal therapy on the oral microbiome and host response related to cognitive parameters may be suggested and should be elucidated in further clinical trials.

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“…Ragarding its effects on the skeletal system, salvianolic acid B promotes new bone formation and protects against oxidative damage (Kayalar et al 2020 ; Xiao et al 2020 ; Bian and Xiang 2020 ); it improves atherosclerosis by inhibiting the YAP/TAZ/JNK signaling pathway in endothelial cells and pericytes (Yang et al 2020 ). In the nervous system, salvianolic acid B could improve the cognitive impairment of mice infected with Porphyromonas gingivalis by inhibiting neuroinflammation and reducing Aβ level (Liu et al 2020 ). Salvianolic acid B can also improve chronic mild stress-induced depressive behaviors in rats via the AMPK/SIRT1 signaling pathway (Liao et al 2020 ).…”

Section: Trpcs Antagonistsmentioning

confidence: 99%

Canonical transient receptor potential channels and their modulators: biology, pharmacology and therapeutic potentials

et al. 2021

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Canonical transient receptor potential channels (TRPCs) are nonselective, high calcium permeability cationic channels. The TRPCs family includes TRPC1, TRPC2, TRPC3, TRPC4, TRPC5, TRPC6, and TRPC7. These channels are widely expressed in the cardiovascular and nervous systems and exist in many other human tissues and cell types, playing several crucial roles in the human physiological and pathological processes. Hence, the emergence of TRPCs modulators can help investigate these channels’ applications in health and disease. It is worth noting that the TRPCs subfamilies have structural and functional similarities, which presents a significant difficulty in screening and discovering of TRPCs modulators. In the past few years, only a limited number of selective modulators of TRPCs were detected; thus, additional research on more potent and more selective TRPCs modulators is needed. The present review focuses on the striking desired therapeutic effects of TRPCs modulators, which provides intel on the structural modification of TRPCs modulators and further pharmacological research. Importantly, TRPCs modulators can significantly facilitate future studies of TRPCs and TRPCs related diseases.

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Salvianolic Acid B improves cognitive impairment by inhibiting neuroinflammation and decreasing Aβ level in Porphyromonas gingivalis-infected mice

Cited by 25 publications

References 58 publications

Porphyromonas gingivalis-Induced Cognitive Impairment Is Associated With Gut Dysbiosis, Neuroinflammation, and Glymphatic Dysfunction

Porphyromonas gingivalis-Induced Cognitive Impairment Is Associated With Gut Dysbiosis, Neuroinflammation, and Glymphatic Dysfunction

Periodontal microorganisms and Alzheimer disease – A causative relationship?

Canonical transient receptor potential channels and their modulators: biology, pharmacology and therapeutic potentials

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