Melatonin: a potential therapeutic approach for the management of primary Sjögren’s syndrome

Liu, Yi; Tan, Ya-Qin; Zhou, Gang

doi:10.1007/s12026-023-09360-w

Cited by 4 publications

(1 citation statement)

References 155 publications

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“…This synthesis occurs primarily in the pineal gland (Ebrahimi et al, 2023;Suzen, 2023). Previous studies have shown that melatonin has several pharmacological effects, including reducing oxidative stress levels, regulating circadian rhythms, preventing apoptosis, and reducing inflammation (Liu et al, 2023b;Rahman and Yang, 2023). The neuroprotective benefits of melatonin in experimental stroke models are well documented.…”

Section: Introductionmentioning

confidence: 99%

Melatonin: a promising neuroprotective agent for cerebral ischemia-reperfusion injury

Tozihi

Shademan

Yousefi

et al. 2023

Front. Aging Neurosci.

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Cerebral ischemia-reperfusion (CIR) injury is initiated by the generation of reactive oxygen species (ROS), which leads to the oxidation of cellular proteins, DNA, and lipids as an initial event. The reperfusion process impairs critical cascades that support cell survival, including mitochondrial biogenesis and antioxidant enzyme activity. Failure to activate prosurvival signals may result in increased neuronal cell death and exacerbation of CIR damage. Melatonin, a hormone produced naturally in the body, has high concentrations in both the cerebrospinal fluid and the brain. However, melatonin production declines significantly with age, which may contribute to the development of age-related neurological disorders due to reduced levels. By activating various signaling pathways, melatonin can affect multiple aspects of human health due to its diverse range of activities. Therefore, understanding the underlying intracellular and molecular mechanisms is crucial before investigating the neuroprotective effects of melatonin in cerebral ischemia-reperfusion injury.

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Section: Introductionmentioning

confidence: 99%

Melatonin: a promising neuroprotective agent for cerebral ischemia-reperfusion injury

Tozihi

Shademan

Yousefi

et al. 2023

Front. Aging Neurosci.

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Berberine safeguards sepsis‐triggered acute gastric damage and inhibits pyroptosis in gastric epithelial cells via suppressing the ubiquitination and degradation of Nrf2

Xie,

Liu,

Chen

et al. 2024

The Kaohsiung J of Med Scie

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Berberine (BBR), a widely recognized traditional Chinese medicine, has attracted considerable attention for its promising anti‐inflammatory effects. The activation of nuclear factor erythroid 2‐related factor 2 (Nrf2) effectively safeguards against organ damage stemming from sepsis‐induced oxidative stress and inflammatory responses. This study examined the potential of BBR in alleviating sepsis‐induced acute gastric injury, with a particular focus on elucidating whether its mechanism of action involves the activation of the Nrf2 signaling pathway. Following intraperitoneal injection of BBR, mice were subjected to the cecal ligation and puncture (CLP) method to induce sepsis. In vitro experiments involved pre‐treating the normal gastric epithelial cells (GES‐1) with BBR, followed by treatment with lipopolysaccharide (LPS). Functional assays were then performed to assess cell proliferation and apoptosis. To validate the role of Nrf2 in pyroptosis and inflammation, siRNA targeting Nrf2 (si‐Nrf2) was transfected into LPS‐treated GES‐1 cells. Additionally, mice were administered the Nrf2 inhibitor ML385 to confirm the protective effects of BBR in vivo. BBR displayed a dose‐dependent effect in mitigating gastric tissue damage, suppressing the release of inflammatory cytokines, and reducing the expression of NLRP3, ASC, and GSDMD‐N. In vitro, BBR fostered GES‐1 cell proliferation, hindered apoptosis, and suppressed the levels of TNF‐α, IL‐18, IL‐1β, NLRP3, ASC, and GSDMD‐N. Further analysis revealed that knocking down Nrf2 reversed BBR's inhibitory effect on pyroptosis in LPS‐treated GES‐1 cells. Through binding to Keap1, BBR efficiently prevented the ubiquitination and degradation of Nrf2, ultimately promoting its nuclear translocation. In vivo experiments confirmed that ML385 reversed the protective effect of BBR on pyroptosis and inflammation. Our research reveals that BBR interacts with Keap1 to activate the Keap1/Nrf2 signaling pathway in gastric epithelial cells, thereby suppressing pyroptosis and inflammation in sepsis‐induced acute gastric injury.

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USP18-mediated protein stabilization of NOTCH1 is associated with altered Th17/Treg cell ratios and B cell-mediated autoantibody secretion in Sjögren syndrome

Jin,

Bai,

et al. 2024

Immunol Res

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Melatonin: a potential therapeutic approach for the management of primary Sjögren’s syndrome

Cited by 4 publications

References 155 publications

Melatonin: a promising neuroprotective agent for cerebral ischemia-reperfusion injury

Melatonin: a promising neuroprotective agent for cerebral ischemia-reperfusion injury

Berberine safeguards sepsis‐triggered acute gastric damage and inhibits pyroptosis in gastric epithelial cells via suppressing the ubiquitination and degradation of Nrf2

USP18-mediated protein stabilization of NOTCH1 is associated with altered Th17/Treg cell ratios and B cell-mediated autoantibody secretion in Sjögren syndrome

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