Anti-inflammatory effects of crocin and crocetin in rat brain microglial cells

Nam, Kyong Nyon; Park, Young-Min; Jung, Hoon-Ji; Lee, Jung Yeon; Min, Booki; Park, Seong-Uk; Jung, Woon Won; Cho, Ki-Ho; Park, Ji-Ho; Kang, Insug; Hong, Joung-Woo; Lee, Eunjoo H.

doi:10.1016/j.ejphar.2010.09.003

Cited by 343 publications

(206 citation statements)

References 36 publications

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“…Our findings showed that crocin, when administered alone, did not produce any change in the protein expression level of iNOS. This finding is in agreement with a previous study showing that crocin, when administered alone, caused no change in basal NO level in microglial cells but markedly protected these cells against LPS-induced inflammation (Nam et al, 2010). These findings suggest that the beneficial gastroprotective effect exerted by crocin is partly mediated by inhibition of iNOS protein expression.…”

Section: Discussionsupporting

confidence: 83%

A preliminary study of the anti-inflammatory and anti-apoptotic effects of crocin against gastric ischemia-reperfusion injury in rats

Mard

Nikraftar

Farbood

et al. 2015

Braz. J. Pharm. Sci.

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The aim of the present study was to investigate the protective effect of crocin on gastric mucosal lesions caused by ischemia-reperfusion (I/R) injury in rats. Thirty-two male rats were randomly divided into sham, I/R, I/R + crocin pretreatment and crocin alone groups. To induce I/R lesions, the celiac artery was clamped for 30 min, and the clamp was then removed to allow reperfusion for 3 h. Crocin-pretreated rats received crocin (15 mg/kg, i.p.) 30 min prior to the induction of I/R injury. Samples of gastric mucosa were collected to quantify the protein expression of caspase-3, an apoptotic factor, and inducible nitric oxide synthase (iNOS), a pro-inflammatory protein, by Western blot. Pretreatment with crocin decreased the total area of gastric lesions and decreased the protein expression levels of caspase-3 and iNOS induced by I/R injury. Our findings showed a protective effect of crocin in gastric mucosa against I/R injury. This effect of crocin was mainly mediated by reducing the protein expression of iNOS and caspase-3. Uniterms:Crocin/protective effect. Gastric mucosal/lesions/ ischemia-reperfusion. Gastric lesions/ treatment/experimental study. Caspase-3. Inducible nitric oxide synthase.O objetivo do presente estudo foi investigar o efeito protetor da crocina em lesões da mucosa gástrica causadas por isquemia-reperfusão (I/R) em ratos. Trinta e dois ratos machos aleatoriamente divididos em grupos de ratos normais, operados como controle, I/R. I/R + pré-tratamento com crocina e crocina sozinha. Para induzir lesões I/R, a artéria celíaca foi grampeada durante 30 minutos e, em seguida, o grampo foi removido para permitir a reperfusão por 3 h. Ratos com pré-tratamento com crocina receberam crocina (15 mg/kg, ip) 30 minutos antes da indução do dano I/R. Amostras de mucosa gástrica foram coletadas para qiuantificar a expressão da proteína da caspase-3, o fator apoptótico, e óxido nítrico sintase induzível (iNOS), uma proteína anti-inflamatória, pela técnica de Western Blot. O pré-tratamento com crocina diminuiu a área total de lesões gástricas e a expressão de níveis de caspase-3 e iNOS induzidas pelo dano I/R. Nossos resultados mostraram o efeito protetor da crocina na mucosa gástrica contra o dano I/R. Este efeito foi mediado, principalmente, por diminuição da expressão das proteínas iNOS e caspase-3.Unitermos: Crocina/efeito protetor. Mucosa gástrica/lesão/isquemia-reperfusão. Lesões gástricas/ tratamento/estudo experimental. Caspase-3. Óxido nítrico sintase induzível.

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Section: Discussionsupporting

confidence: 83%

A preliminary study of the anti-inflammatory and anti-apoptotic effects of crocin against gastric ischemia-reperfusion injury in rats

Mard

Nikraftar

Farbood

et al. 2015

Braz. J. Pharm. Sci.

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“…Crocin has been shown to exert neuroprotective effects in several model systems, possibly through suppression of free radical production (50)(51)(52). More recently, crocin has been reported to suppress microglial activation (53) and ER stress (54). The MS animal model, EAE, also showed evidence of ER stress gene activation including XBP-1/s, BiP, PERK, and CHOP, together with inflammatory gene expression in diseased spinal cords, which was suppressed by crocin treatment and accompanied by substantial improvements in disease outcomes.…”

Section: Discussionmentioning

confidence: 99%

Neuroinflammation and Endoplasmic Reticulum Stress Are Coregulated by Crocin To Prevent Demyelination and Neurodegeneration

Deslauriers

Afkhami-Goli

Paul

et al. 2011

The Journal of Immunology

112

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Endoplasmic reticulum (ER) stress is a homeostatic mechanism, which is used by cells to adapt to intercellular and intracellular changes. Moreover, ER stress is closely linked to inflammatory pathways. We hypothesized that ER stress is an integral component of neuroinflammation and contributes to the development of neurological diseases. In autopsied brain specimens from multiple sclerosis (MS) and non-MS patients, XBP-1 spliced variant (XBP-1/s) was increased in MS brains (p < 0.05) and was correlated with the expression of the human endogenous retrovirus-W envelope transcript, which encodes the glycoprotein, Syncytin-1 (p < 0.05). In primary human fetal astrocytes transfected with a Syncytin-1–expressing plasmid, XBP-1/s, BiP, and NOS2 were induced, which was suppressed by crocin treatment (p < 0.05). Crocin also protected oligodendrocytes exposed to cytotoxic supernatants derived from Syncytin-1–expressing astrocytes (p < 0.05) and NO-mediated oligodendrocytotoxicity (p < 0.05). During experimental autoimmune encephalomyelitis (EAE), the transcript levels of the ER stress genes XBP-1/s, BiP, PERK, and CHOP were increased in diseased spinal cords compared with healthy littermates (p < 0.05), although CHOP expression was not involved in the EAE disease phenotype. Daily treatment with crocin starting on day 7 post-EAE induction suppressed ER stress and inflammatory gene expression in spinal cords (p < 0.05), which was accompanied by preserved myelination and axonal density, together with reduced T cell infiltration and macrophage activation. EAE-associated neurobehavioral deficits were also ameliorated by crocin treatment (p < 0.05). These findings underscored the convergent roles of pathogenic ER stress and immune pathways in neuroinflammatory disease and point to potential therapeutic applications for crocin.

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“…This inhibition was associated with reduced cell proliferation through the downregulation or upregulation of certain apoptotic proteins, including cytochrome c and cleaved caspase-3 expression. In addition, a number of pharmacological studies have demonstrated crocetin to have multiple activities, including anti-inflammatory (35,36) and anti-oxidant (37,38) effects. Therefore, it was hypothesized that the anti-oxidant and anti-inflammatory effects of crocetin may also be considered to be involved in several synergistic antitumor mechanisms (39,40).…”

Section: D a Bmentioning

confidence: 99%

Crocetin induces apoptosis of BGC-823 human gastric cancer cells

Wang

et al. 2013

Molecular Medicine Reports

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Abstract. Gastric cancer (GC) is one of the most common types of gastrointestinal tumors worldwide, and the side effects of chemotherapeutic drugs and the resistance to chemotherapy remain problematic in its clinical treatment. Therefore, safe and effective novel agents are urgently required. The purpose of the present study was to investigate the crocetin-sensitive treatment of GC and its possible mechanisms. BGC-823 human GC cells were treated with crocetin. The effects of crocetin on the viability of the cells were determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Hoechst 33258 dyeing and Rh123 staining were used to detect cell apoptosis. The BGC-823 cells were subjected to western blotting analysis for detection of cytochrome c and cleaved caspase-3 protein expression. Crocetin inhibited the proliferation of the GC cell line in a dose-and time-dependent manner. Apoptotic BGC-823 cells induced by crocetin were stained by Hoechst 33258 and observed under a light microscope for cell membrane staining of dense nuclei, nuclear pyknosis, fragmentation, chromatin condensation and highlighted nuclear membrane staining. This revealed a decline in the mitochondrial membrane potential of the BGC-823 cells. Crocetin also induced caspase-3 activation and cytochrome c translocation into the cytosol from the mitochondria. The results of this study indicate that crocetin induces the apoptosis of BGC-823 cells, and may be used as an effective agent in the treatment of GC.

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Anti-inflammatory effects of crocin and crocetin in rat brain microglial cells

Cited by 343 publications

References 36 publications

A preliminary study of the anti-inflammatory and anti-apoptotic effects of crocin against gastric ischemia-reperfusion injury in rats

A preliminary study of the anti-inflammatory and anti-apoptotic effects of crocin against gastric ischemia-reperfusion injury in rats

Neuroinflammation and Endoplasmic Reticulum Stress Are Coregulated by Crocin To Prevent Demyelination and Neurodegeneration

Crocetin induces apoptosis of BGC-823 human gastric cancer cells

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