Hydrogen Sulfide Ameliorates Lipopolysaccharide-Induced Memory Impairment in Mice by Reducing Apoptosis, Oxidative, and Inflammatory Effects

Kshirsagar, Viplav; Thingore, Chetan; Gursahani, Malvika; Gawali, Nitin B.; Juvekar, Archana R.

doi:10.1007/s12640-021-00374-6

Cited by 18 publications

(7 citation statements)

References 90 publications

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“…The administration of LPS causes inflammatory response mediated mainly by TLR4, microglial reactivation and neuroinflammation, which results in the degeneration of neurons, synaptic loss and finally neuronal cell death [ 70 ]. This process is mediated by production of inflammatory molecules, such as TNF-α, IL-6, and IL-1β, increased activity of iNOS, COX-2, β-secretase, γ-secretase, Aβ accumulation and oxidative stress [ 70 , 71 ]. Amyloidogenesis caused by LPS is the most prominent phenomenon in the cortical and hippocampal areas [ 72 ].…”

Section: The Utility Of Lps Inflammation Model In the Research Fieldmentioning

confidence: 99%

“…In patients suffering from neurodegenerative diseases, similar pathomorphological and clinical symptoms are found. Increased Aβ accumulation due to chronic LPS administration makes the LPS model a very adequate method for AD studies [ 71 ]. LPS can also induce characteristic features of PD by causing neuroinflammation and dopaminergic neuron loss [ 73 , 74 ].…”

Section: The Utility Of Lps Inflammation Model In the Research Fieldmentioning

confidence: 99%

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Lipopolysaccharide-Induced Model of Neuroinflammation: Mechanisms of Action, Research Application and Future Directions for Its Use

2022

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Despite advances in antimicrobial and anti-inflammatory therapies, inflammation and its consequences still remain a significant problem in medicine. Acute inflammatory responses are responsible for directly life-threating conditions such as septic shock; on the other hand, chronic inflammation can cause degeneration of body tissues leading to severe impairment of their function. Neuroinflammation is defined as an inflammatory response in the central nervous system involving microglia, astrocytes, and cytokines including chemokines. It is considered an important cause of neurodegerative diseases, such as Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Lipopolysaccharide (LPS) is a strong immunogenic particle present in the outer membrane of Gram-negative bacteria. It is a major triggering factor for the inflammatory cascade in response to a Gram-negative bacteria infection. The use of LPS as a strong pro-inflammatory agent is a well-known model of inflammation applied in both in vivo and in vitro studies. This review offers a summary of the pathogenesis associated with LPS exposure, especially in the field of neuroinflammation. Moreover, we analyzed different in vivo LPS models utilized in the area of neuroscience. This paper presents recent knowledge and is focused on new insights in the LPS experimental model.

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Section: The Utility Of Lps Inflammation Model In the Research Fieldmentioning

confidence: 99%

Section: The Utility Of Lps Inflammation Model In the Research Fieldmentioning

confidence: 99%

Lipopolysaccharide-Induced Model of Neuroinflammation: Mechanisms of Action, Research Application and Future Directions for Its Use

2022

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“…Timely monitoring of apoptosis is helpful for early warning and therapy of related pathophysiological processes and the continuous assessment of drug effectiveness. H 2 S has been found to protect cells: H 2 S can prevent Abeta-induced neuronal apoptosis by diminishing mitochondrial translocation of phosphatase and tensin homolog deleted on chromosome ten (PTEN) (Cui Z et al, 2016); H 2 S can restrain cell apoptosis and protect bronchial epithelium in a mouse model of allergic inflammation (Mendes et al, 2019); H 2 S improves LPS-induced memory disorder in mice by decreasing apoptosis, oxidation, and inflammatory effects (Kshirsagar et al, 2021). However, H 2 S can also promote apoptosis: H 2 S contributes to LPS-induced osteoblast apoptosis by restraining the AKT/NF-κB signaling pathway (Wang et al, 2020); H 2 S, which releases whey protein derivatives, induces apoptosis through extrinsic and intrinsic pathways (Li et al, 2020).…”

Section: Apoptosis Imagingmentioning

confidence: 99%

H2S-based fluorescent imaging for pathophysiological processes

Jia

Zhang²,

Hou³

et al. 2023

Front. Chem.

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Hydrogen sulfide (H2S), as an important endogenous signaling molecule, plays a vital role in many physiological processes. The abnormal behaviors of hydrogen sulfide in organisms may lead to various pathophysiological processes. Monitoring the changes in hydrogen sulfide is helpful for pre-warning and treating these pathophysiological processes. Fluorescence imaging techniques can be used to observe changes in the concentration of analytes in organisms in real-time. Therefore, employing fluorescent probes imaging to investigate the behaviors of hydrogen sulfide in pathophysiological processes is vital. This paper reviews the design strategy and sensing mechanisms of hydrogen sulfide-based fluorescent probes, focusing on imaging applications in various pathophysiological processes, including neurodegenerative diseases, inflammation, apoptosis, oxidative stress, organ injury, and diabetes. This review not only demonstrates the specific value of hydrogen sulfide fluorescent probes in preclinical studies but also illuminates the potential application in clinical diagnostics.

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“…In addition to the inhibition of LPS-induced neuroinflammation and oxidative stress upon LPS exposure in mice, H 2 S also reduced neuronal apoptosis through the modulation of c-Jun and caspase 3 activation [ 110 ].…”

Section: Endogenous Neurotoxicantsmentioning

confidence: 99%

Hydrogen Sulfide (H2S) Signaling as a Protective Mechanism against Endogenous and Exogenous Neurotoxicants

Aschner

Skalny

Tang

et al. 2022

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In view of significant role of H2S in brain functioning through, it is proposed that H2S may also possess protective effects against adverse effects of neurotoxicants. Therefore, the objective of the present review is discussion of neuroprotective effects of H2S against toxicity of a wide spectrum of endogenous and exogenous agents, involved in pathogenesis of neurological diseases as etiological factors or key players in disease pathogenesis. Generally, the existing data demonstrate that H2S possesses neuroprotective effects upon exposure to endogenous (amyloid β, glucose and advanced-glycation end-products, homocysteine, lipopolysaccharide, and ammonia) and exogenous (alcohol, formaldehyde, acrylonitrile, metals, 6-hydroxydopamine, as well as 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) and its metabolite 1-methyl-4-phenyl pyridine ion (MPP) neurotoxicants. On the one hand, neuroprotective effects are mediated by S-sulfhydration of key regulators of antioxidant (Sirt1, Nrf2) and inflammatory response (NF-κB) resulting in modulation of the downstream signaling, such as SIRT1/TORC1/CREB/BDNF-TrkB, Nrf2/ARE/HO-1, or other pathways. On the other hand, H2S appears to possess direct detoxicative effect through binding of endogenous (ROS, AGEs, Aβ) and exogenous (MeHg) neurotoxicants, thus reducing their toxicity. Moreover, alteration of H2S metabolism through inhibition of H2S-synthetizing enzymes in brain (CBS, 3-MST) may be considered as a significant mechanism of neurotoxicity. Taken together, the existing data indicate that modulation of cerebral H2S metabolism may be used as a neuroprotective strategy to counteract neurotoxicity of a wide spectrum of endogenous and exogenous neurotoxicants associated with neurodegeneration (Alzheimer’s and Parkinson’s disease), fetal alcohol syndrome, hepatic encephalopathy, environmental neurotoxicant exposure, etc. In this particular case, modulation of H2S-synthetizing enzymes or the use of H2S-releasing drugs should be considered as the potential tools, although particular efficiency and safety of such interventions are to be addressed in further studies.

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Hydrogen Sulfide Ameliorates Lipopolysaccharide-Induced Memory Impairment in Mice by Reducing Apoptosis, Oxidative, and Inflammatory Effects

Cited by 18 publications

References 90 publications

Lipopolysaccharide-Induced Model of Neuroinflammation: Mechanisms of Action, Research Application and Future Directions for Its Use

Lipopolysaccharide-Induced Model of Neuroinflammation: Mechanisms of Action, Research Application and Future Directions for Its Use

H2S-based fluorescent imaging for pathophysiological processes

Hydrogen Sulfide (H2S) Signaling as a Protective Mechanism against Endogenous and Exogenous Neurotoxicants

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