Aloin Suppresses Lipopolysaccharide-Induced Inflammatory Response and Apoptosis by Inhibiting the Activation of NF-κB

Luo, Xuan; Zhang, Haowei; Wei, Xiduan; Shi, Mengjuan; Fan, Ping; Xie, Weidong; Zhang, Yaou; Xu, Ning

doi:10.3390/molecules23030517

Cited by 41 publications

(32 citation statements)

References 49 publications

(49 reference statements)

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“…Luo et al ( 35 ) demonstrated that aloin attenuated LPS-induced NF-κB transcriptional activity by inhibiting its upstream kinase p38 MAPK and mitogen- and stress-activated protein kinase-1. However, the results of the present study demonstrated that aloin pretreatment had no effect on LPS-induced p38 activation.…”

Section: Discussionmentioning

confidence: 99%

Aloin suppresses lipopolysaccharide‑induced inflammation by inhibiting JAK1‑STAT1/3 activation and ROS production in RAW264.7 cells

Tang

Sheng

et al. 2018

Int J Mol Med

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The anti-inflammatory effects of aloin, a bioactive ingredient extracted from Aloe vera, have been described previously. The present study aimed to assess these effects and explore the underlying molecular mechanisms. RAW264.7 cells were incubated with different doses of aloin (100, 150 and 200 µg/ml) and lipopolysaccharide (LPS; 100 ng/ml) for the indicated times. Then, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 expression levels were detected by western blot analysis and reverse transcription polymerase chain reaction (RT-PCR). The concentrations of inflammatory cytokines in the cell culture supernatant were determined by ELISA. Total nitric oxide (NO) assay and reactive oxygen species (ROS) kits were used to detect NO and ROS levels, respectively. Mitogen-activated protein kinase, nuclear factor κB and Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway activation were verified by western blot analysis. Confocal and nucleocytoplasmic separation experiments were used to detect STAT nuclear translocation. It was identified that aloin decreased the level of LPS-induced iNOS expression, inhibiting the release of interleukin (IL)-1β, IL-6, tumour necrosis factor-α and NO dose-dependently. Mechanistically, aloin suppressed LPS-induced JAK1-STAT1/3 activation and STAT1/3 nuclear translocation. Additionally, LPS-induced ROS production was inhibited by aloin. Collectively, these data suggest that aloin attenuated LPS-induced inflammation by inhibiting ROS-mediated activation of the JAK1-STAT1/3 signalling pathway, thereby inhibiting the nuclear translocation of STAT1/3 in RAW264.7 cells. The present study provides an experimental basis for the clinical application of aloin in inflammatory-associated diseases.

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Section: Discussionmentioning

confidence: 99%

Aloin suppresses lipopolysaccharide‑induced inflammation by inhibiting JAK1‑STAT1/3 activation and ROS production in RAW264.7 cells

Tang

Sheng

et al. 2018

Int J Mol Med

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“…Aloin (ALO) is a bioactive component that is extracted from aloe vera. It has been reported to have anti-inflammatory, 1,2 anti-oxidant, 3 and anti-tumour effects. 4,5 In addition, ALO has been reported to inhibit proliferation and induce the apoptosis of various tumour cells.…”

Section: Introductionmentioning

confidence: 99%

“…4,5 In addition, ALO has been reported to inhibit proliferation and induce the apoptosis of various tumour cells. 1,5,6 However, the molecular mechanism(s) underlying ALO's anti-cancer activity remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

<p>Aloin Inhibits the Proliferation and Migration of Gastric Cancer Cells by Regulating NOX2–ROS-Mediated Pro-Survival Signal Pathways</p>

Wang¹,

Tang²,

Wang³

et al. 2020

DDDT

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Background: Aloin has been reported to have many pharmacological effects including antiinflammatory, anti-oxidant and anti-tumour activities. However, the precise molecular mechanisms underlying the anti-tumour properties of aloin are yet to be elucidated. Methods: HGC-27 and BGC-823 gastric cancer cells were treated with aloin. EdU and colony formation assays were used to detect the proliferation ability of cells. The migration of cells was detected using wound healing and transwell assays. Western blotting was used to detect the levels of cyclinD1, cyclin E1, MMPs, N-cadherin, E-cadherin and NOX2. The phosphorylation of Akt, mTOR, P70S6K, S6, Src, stat3 and IκBα were also detected by Western blotting. Flow cytometry was used to detect the cell cycle distribution.The location of p65 in cells was determined by using a confocal microscopy assay. The total amounts of ROS present in cells were measured using an ROS assay kit. Results: Here, we found that aloin inhibited the proliferation and migration of HGC-27 and BGC-823 gastric cancer cells using a combination of EdU, colony formation, wound healing and transwell assays. Further investigations revealed that aloin decreased the protein expression levels of cyclin D1, N-cadherin, and the matrix metalloproteinases (MMP)-2 and MMP-9; increased E-cadherin expression in a dose-dependent manner; inhibited reactive oxygen species (ROS) generation; and mediated the activation of Akt-mTOR, signal transducer and activator of transcription-3 (Stat3), and NF-κB signalling pathways. Our results also indicated that aloin is able to attenuate the expression levels of the two regulatory proteins of nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2), p47 phox and p22 phox , but had no effect on the level of gp91 phox. N-acetylcysteine treatment of gastric cancer cells inhibited ROS production and Akt-mTOR, Stat3, and IκBα phosphorylation. Taken together, our data suggest that aloin inhibits the proliferation and migration of gastric cancer cells by downregulating NOX2-ROS-mediated activation of the Akt-mTOR, Stat3, and NF-κB signalling pathways. Conclusion: Our findings suggest a potential role for aloin in the prevention of gastric cancer cell proliferation and migration and provide novel insights into the anti-cancer properties of aloin.

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“…Furthermore, it has been reported that inflammatory cells play an important role in neurodegenerative diseases via release of various pro‐inflammatory molecules (Calabrese et al., ). For example, NO is a labile molecule that has been associated with numerous pathological processes, and it is produced by iNOS, which is locally secreted by inflammatory stimuli (Luo et al., ). In addition, the pro‐inflammatory cytokines IL‐6, TNF‐α and IL‐1β are potent enhancers of neuroinflammatory reactions and are involved in demyelination and neuronal damage (Yu et al., ).…”

Section: Discussionmentioning

confidence: 99%

“…For example, NO is a labile molecule that has been associated with numerous pathological processes, and it is produced by iNOS, which is locally secreted by inflammatory stimuli (Luo et al, 2018). In addition, the pro-inflammatory cytokines IL-6, TNF-and IL-1 are potent enhancers of neuroinflammatory reactions and are involved in demyelination and neuronal damage (Yu et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Therapeutic effect of oligomeric proanthocyanidin in cuprizone‐induced demyelination

Wang

Yang

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?Oligomeric proanthocyanidin has the capacity to alleviate abnormalities in neurological functioning. However, whether oligomeric proanthocyanidin can reduce the progression of demyelination or promote remyelination in demyelinating diseases remains unknown. What is the main finding and its importance?Oligomeric proanthocyanidin can improve cuprizone‐induced demyelination by inhibiting immune cell infiltration, reversing overactivated microglia, decreasing the inflammatory cytokines secreted by inflammatory cells and decreasing the production of myelin oligodendrocyte glycoprotein35–55‐specific antibody in the brain. Abstract Demyelinating diseases of the CNS, including multiple sclerosis, neuromyelitis optica and acute disseminated encephalomylitis, are characterized by recurrent primary demyelination–remyelination and progressive neurodegeneration. In the present study, we investigated the therapeutic effect of oligomeric proanthocyanidin (OPC), the most effective component of grape seed extract, in cuprizone‐fed C57BL/6 mice, a classic demyelination–remyelination model. Our results showed that OPC attenuated abnormal behaviour, reduced demyelination and increased expression of myelin basic protein and expression of O4+ oligodendrocytes in the corpus callosum. Oligomeric proanthocyanidin also reduced the numbers of B and T cells, activated microglia in the corpus callosum and inhibited secretion of inflammatory factors. Furthermore, concentrations of myelin oligodendrocyte glycoprotein‐specific antibodies were significantly reduced in serum and brain homogenates after OPC treatment. Together, these results demonstrate a potent therapeutic effect for OPC in cuprizone‐mediated demyelination and clearly highlight multiple effects of this natural product in attenuating myelin‐specific autoantibodies and the inflammatory microenvironment in the brain.

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Aloin Suppresses Lipopolysaccharide-Induced Inflammatory Response and Apoptosis by Inhibiting the Activation of NF-κB

Cited by 41 publications

References 49 publications

Aloin suppresses lipopolysaccharide‑induced inflammation by inhibiting JAK1‑STAT1/3 activation and ROS production in RAW264.7 cells

Aloin suppresses lipopolysaccharide‑induced inflammation by inhibiting JAK1‑STAT1/3 activation and ROS production in RAW264.7 cells

<p>Aloin Inhibits the Proliferation and Migration of Gastric Cancer Cells by Regulating NOX2–ROS-Mediated Pro-Survival Signal Pathways</p>

Therapeutic effect of oligomeric proanthocyanidin in cuprizone‐induced demyelination

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