Sirtuin 1 alleviates endoplasmic reticulum stress-mediated apoptosis of intestinal epithelial cells in ulcerative colitis

Ren, Mengting; Gu, Meng-Li; Zhou, Xinxin; Yu, Mosang; Pan, Hanghai; Ji, Feng; Ding, Chen-Yan

doi:10.3748/wjg.v25.i38.5800

Cited by 59 publications

(42 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[10][11][12] SIRT1 is activated in many central nervous system diseases, such as subarachnoid haemorrhage and Parkinson's disease. 13 In addition, it has been reported that it is an important…”

mentioning

confidence: 99%

Sirtuin 1 alleviates neuroinflammation‐induced apoptosis after traumatic brain injury

Guan

Wang

Wu³

et al. 2021

J Cellular Molecular Medi

View full text Add to dashboard Cite

The pathophysiological features of traumatic brain injury (TBI) include primary brain injuries, which are difficult to predict, and secondary brain injury. 1,2 Over the course of TBI, neuronal apoptosis occurs through a complex sequence of pathological events that involve several contributing factors, such as excitotoxicity, excitotoxic damage, mitochondrial dysfunction and autophagy. 3 Among these events, inflammation is an important factor that aggravates nerve injury during the process of secondary insult. Although the exact mechanisms responsible for the occurrence of neuronal insult and their final degeneration are equivocal, vast literature suggests an important role of neuroinflammation. 4,5 Cytokine signalling and inflammasome are linked to the 'redox-sensitive' master transcriptional regulator nuclear factor-kappa B (NF-κB). Indeed, activation of NF-κB causes an increase in the interleukin (IL)-1 level, which promotes the cascade of inflammatory factors in microglia (ie TNFα) and astrocytes (ie IL-6). 6,7 Accordingly, restrained activation of NF-κB reduces the neuroinflammatory process, which can prevent neuronal apoptosis. 8 Sirtuin 1 (SIRT1), also known as nicotinamide adenine dinucleotide (NAD)-dependent deacetylase sirtuin-1, contributes to cellular regulation (reaction to stressors and longevity). 9 It is a highly conserved and well-characterized NAD-dependent class III histone deacetylase in mammalian cells. Numerous studies have demonstrated that SIRT1 plays a central role in the regulation of different biological processes, such as mitochondrial biogenesis, oxidation and inflammation. [10][11][12] SIRT1 is activated in many central nervous system diseases, such as subarachnoid haemorrhage and Parkinson's disease. 13 In addition, it has been reported that it is an important

show abstract

mentioning

confidence: 99%

Sirtuin 1 alleviates neuroinflammation‐induced apoptosis after traumatic brain injury

Guan

Wang

Wu³

et al. 2021

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…SRT1720 is a strong SIRT1 activator that has been used in a variety of experimental studies [ 30 ]. The anti-inflammatory and anti-apoptotic effects of SRT1720 have been observed both in vivo and in vitro [ 31 , 32 ]. In the present study, we found that treatment with the SIRT1 activator SRT1720 significantly alleviated LPS/D-Gal-induced fulminant hepatitis and improved the survival rate of the experimental animals, suggesting that SRT1720 might have potential value for the control of fulminant hepatitis, a life-threatening condition.…”

Section: Discussionmentioning

confidence: 99%

The sirtuin 1 activator SRT1720 alleviated endotoxin-induced fulminant hepatitis in mice

Zhou

Yang

et al. 2021

Exp. Anim.

View full text Add to dashboard Cite

The metabolic sensor sirtuin 1 (SIRT1) also functions as a checkpoint in inflammation, and SRT1720 is a highly active and selective SIRT1 activator shown to alleviate inflammatory injury in several recent experimental studies. In the present study, the potential effects and underlying mechanisms of SRT1720 on lipopolysaccharide (LPS)-induced fulminant hepatitis in D-galactosamine (D-Gal)-sensitized mice were investigated. The results indicated that treatment with SRT1720 inhibited LPS/D-Gal-induced elevation of ALT and AST, alleviated the histological abnormalities, suppressed the induction of TNF-α and IL-6, mitigated the phosphorylation of JNK, downregulated the activities of caspase 8, caspase 9 and caspase 3, decreased the level of cleaved caspase 3, reduced the TUNEL-positive cells, and improved the survival rate of the LPS/D-Gal-exposed mice. These data indicated that treatment with the SIRT1 activator SRT1720 alleviated LPS/D-Gal-induced fulminant hepatitis, which might be attributed to the suppressive effects of SRT1720 on TNF-α production and the subsequent activation of the apoptosis cascade.

show abstract

“…CHOP is a key molecule in the downstream of PERK, and ER stress can be mediated by the PERK-CHOP pathway [11]. Caspase-12 is another marker of ER stress which is cleaved into active fragment on ER stress [22].The augment of these ER stress markers is considered to correlate with increased calcium level and directly destroys the balance of calcium homeostasis which is another important characteristic of AD [5,12,16]. Results in our study showed the decrease in the expression of GRP78, CHOP and cleaved caspase-12 after treatment of schisandrin which indicated the positive effect of schisandrin on ER stress.…”

Section: Discussionmentioning

confidence: 99%

“…SIRT1 has been reported to relieve the ER stress and inflammation [1]. It is demonstrated that SIRT1 may alleviate the ER stress-regulated apoptosis via the decreased expression of CHOP and inactivation of caspase-12 [22]. Moreover, SIRT1 suppresses the ER stress through the mediation of eIF2α deacetylation [20].…”

Section: Discussionmentioning

confidence: 99%

Schisandrin ameliorates cognitive deficits, endoplasmic reticulum stress and neuroinflammation in streptozotocin (STZ)-induced Alzheimer’s disease rats

et al. 2020

View full text Add to dashboard Cite

Schisandrin, an active component extracted from Schisandra chinensis (Turcz.) Baill has been reported to alleviate the cognitive impairment in neurodegenerative disorder like Alzheimer's disease (AD). However, the mechanism by which schisandrin regulates the cognitive decline is still unclear. In our study, intracerebroventricular injection of streptozotocin (STZ) was employed to establish AD model in male Wistar rats, and indicated dose of schisandrin was further administered. The Morris water maze test was performed to evaluate the ability of learning and memory in rats with schisandrin treatment. The results indicated that schisandrin improved the capacity of cognition in STZ-induced rats. The contents of pro-inflammatory cytokines in brain tissue were determined by ELISA, and the expressions of these cytokines were assessed by western-blot and immunohistochemistry. The results showed that treatment of schisandrin significantly reduced the production of inflammation mediators including tumor necrosis factor-α, interleukin-1β and interleukin-6. Further study suggested a remarkable decrease in the expressions of ER stress maker proteins like C/EBP-homologous protein, glucose-regulated protein 78 and cleaved caspase-12 in the presence of schisandrin, meanwhile the up-regulation of sirtuin 1 (SIRT1) was also observed in the same group. Additionally, the results of western-blot and EMSA demonstrated that schisandrin inhibited NF-κB signaling in the brain of STZ-induced rats. In conclusion, schisandrin ameliorated STZ-induced cognitive dysfunction, ER stress and neuroinflammation which may be associated with up-regulation of sirtuin 1 (SIRT1). Our study provides novel mechanisms for the neuroprotective effect of 3 schisandrin in AD treatment.

show abstract

Sirtuin 1 alleviates endoplasmic reticulum stress-mediated apoptosis of intestinal epithelial cells in ulcerative colitis

Cited by 59 publications

References 48 publications

Sirtuin 1 alleviates neuroinflammation‐induced apoptosis after traumatic brain injury

Sirtuin 1 alleviates neuroinflammation‐induced apoptosis after traumatic brain injury

The sirtuin 1 activator SRT1720 alleviated endotoxin-induced fulminant hepatitis in mice

Schisandrin ameliorates cognitive deficits, endoplasmic reticulum stress and neuroinflammation in streptozotocin (STZ)-induced Alzheimer’s disease rats

Contact Info

Product

Resources

About