Galactomannan as a Potential Modulator of Intestinal Ischemia–Reperfusion Injury

Stringa, Pablo; Toledano, Víctor; Papa‐Gobbi, Rodrigo; Arreola, Miguel A.; Largo, Carlota; Machuca, Mariana Alejandra; Aguirre, Luis A.; Rumbo, Martı́n; López-Collazo, Eduardo; Oliveros, Francisco Hernández

doi:10.1016/j.jss.2019.10.027

Cited by 9 publications

(10 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Several studies have shown that galactomannan induces endotoxin tolerance in monocytes through binding to its receptor Dectin-1, but without the initial production of cytokines. 37,43 Coinciding with these results, in our study, a lower inflammatory response was observed in the preconditioned groups with galactomannan at the expense of interferon gamma compared with the lipopolysaccharide group ( p < 0.001). In addition, in the preconditioned groups with galactomannan, the median survival was significantly higher compared to the control.…”

Section: Discussionsupporting

confidence: 86%

See 1 more Smart Citation

Induction of Endotoxin Tolerance Delays Acute Rejection in a Hindlimb Transplantation Model in Rats

Yanchuck

Toledano

Bonastre

et al. 2022

Plastic &Amp; Reconstructive Surgery

Self Cite

View full text Add to dashboard Cite

Background: Acute rejection is seen in 85 percent of composite vascular allogeneic transplants despite long-term immunosuppression. Recently, it was reported that the induction of endotoxin tolerance prolonged heart allograft survival in mice. However, it produced side effects in all the animals secondary to the inflammatory reaction. Galactomannan has shown endotoxin tolerance without this side effect in vitro. The authors hypothesized that galactomannaninduced endotoxin tolerance delays acute rejection in vascular allogeneic transplantation without the side effects produced by lipopolysaccharide. Methods: Twenty-four rat hindlimb transplants were divided into four groups according to the preconditioning received: control, lipopolysaccharide (0.16 ml/kg), galactomannan 72 hours before (galactomannan-72) (8 ml/kg), and galactomannan 24 hours before (galactomannan-24) (8 ml/kg). Median acute rejection time, weight loss, and diarrheal episodes were monitored. Blood samples were collected at 0, 7, 21, 30, 45, and 60 days. Plasma cytokines (i.e., tumor necrosis factor alpha, interferon gamma), peripheral chimerism, and lymphocyte percentages were analyzed. Results: Median allograft survival was 40 days (range, 40 to 44 days) in the control group, 68 days (range, 61 to 71 days) in the lipopolysaccharide group, and 70 days (range, 69 to 73 days) in both galactomannan groups (p = 0.001). Weight loss was higher in the lipopolysaccharide group (p < 0.001), as was the 83.3 percent rate of diarrheal episodes (control, 0 percent, p = 0.015; galactomannan-72, 0 percent, p = 0.015; and galactomannan-24, 16.7 percent, p = 0.02). Preconditioned rats had higher peripheral blood chimerism (lipopolysaccharide, 2.30 ± 0.13 percent; galactomannan-72, 2.63 ±1.46 percent; and galactomannan-24, 2.47 ± 0.19 percent) compared to the control group (2.06 ± 0.36 percent) (lipopolysaccharide, p = 0.04; galactomannan-72, p = 0.002; and galactomannan-24, p = 0.002). Conclusions: Induction of endotoxin tolerance delays acute rejection in the rat hindlimb transplantation model. Galactomannan preconditioning has no lipopolysaccharide side effects and was equally effective in delaying acute rejection. (Plast. Reconstr. Surg. 149: 216e, 2022.) Clinical Relevance Statement: The contributions of this experimental work are very incipient. Although the use of galactomannan in clinical practice requires more studies to assess its safety, there is no doubt that immunomodulation may be one of the responses that solve the problem of long-term immunosuppression.

show abstract

Section: Discussionsupporting

confidence: 86%

“…Previous studies established 72 hours as the minimum time required to develop endotoxin tolerance. 34,[41][42][43]…”

Section: Ementioning

confidence: 99%

Induction of Endotoxin Tolerance Delays Acute Rejection in a Hindlimb Transplantation Model in Rats

Yanchuck

Toledano

Bonastre

et al. 2022

Plastic &Amp; Reconstructive Surgery

Self Cite

View full text Add to dashboard Cite

show abstract

“…Webb & Berthel (Fabaceae) galactomannan can reduce the glycemic index of starchy foods [35]. Galactomannan pretreatment constitutes a novel and promising therapy to decrease local and remote damage triggered by intestinal ischemia-reperfusion injury [36]. Chemical structure of galactomannan has shown in Fig.…”

Section: Galactomannansmentioning

confidence: 99%

Diosgenin and galactomannans, natural products in the pharmaceutical sciences

et al. 2021

View full text Add to dashboard Cite

Background Diosgenin is an isospirostane derivative, which is a steroidal sapogenin and the product of acids or enzymes hydrolysis process of dioscin and protodioscin. Galactomannans are heteropolysaccharides composed of D-mannose and D-galactose, which are major sources of locust bean, guar, tara and fenugreek. Methods Literature survey was accomplished using multiple databases including PubMed, Science Direct, ISI web of knowledge and Google Scholar. Results Four major sources of seed galactomannans are locust bean (Ceratonia siliqua), guar (Cyamopsis tetragonoloba), tara (Caesalpinia spinosa Kuntze), and fenugreek (T.foenum-graecum). Diosgenin has effect on immune system, lipid system, inflammatory and reproductive systems, caner, metabolic process, blood system, blood glucose and calcium regulation. The most important pharmacological benefits of galactomannan are antidiabetic, antioxidant, anticancer, anticholinesterase, antiviral activities, and appropriate for dengue virus and gastric diseases. Conclusions Considering the importance of diosgenin and galactomannans, the obtained findings suggest potential of diosgenin and galactomannans as natural products in pharmaceutical industries.

show abstract

“…Intestinal ischemia/reperfusion (II/R)-induced injury is one of the most serious clinical events which result from different pathophysiologic conditions, including burns, trauma, haemorrhagic shock, infection, acute superior mesenteric artery (SMA) occlusion, as well as organ transplantation, which leads to severe injuries in the structure and function of intestinal epithelial cells (IECs) [1][2]. It is an intense local in ammation responses that is produced in the small intestine transiently deprived of blood ow during reperfusion [3][4][5]. More complex mechanisms that trigger in ammation are involved in its development and ampli cation have been identi ed only partially [6-8].…”

Section: Introductionmentioning

confidence: 99%

Intestinal Epithelial Cell Derived Exosomes Package MicroRNA-23a-3p Alleviate Gut Damage After Ischemia/Reperfusion via Targeting MAP4K4

Yang¹,

Zheng

et al. 2021

Preprint

View full text Add to dashboard Cite

Backgroud: Intestinal epithelial cells (IEC) contribute to regulate gut injury after intestinal isochemia/reperfusion (II/R). Exosomes are well documented to deliver bioactive molecules to recipient cells to modulate cell function. However, the role of IEC-derived exosomes in gut damage after II/R and the underlying mechanisms remains unclear. Methods IEC-derived exosomes were intravenously injected into the rats after the superior mesenteric artery occlusion for 45 min following reperfusion for 6h. The scores of gut injury, ZO-1 and IL-17A expression, TNF-α and endotoxin concentration were determined at 3 days after II/R assault. Exosomal microRNA-23a-3p and its downstream target molecule-MAP4K4 were also detected. Results Our results showed that the IEC-derived exosomes attenuated the damage of IECs after oxygen-glucose deprivation in vitro (p<0.05) and the degree of gut injury at 3 days after II/R assault in vivo (p<0.05). Injection of miR-23a-3p knockdown exosomes derived from IECs aggravated the II/R injury whereas PF-6260933, a small-molecule inhibitor of MAP4K4, was partly reversed the injuried degree by intraperitoneal injection. Underlying mechanism studies revealed that exosomal miR-23a-3p attenuated gut damage by regulating its downstream target MAP4K4. Conclusions We demonstrated that IEC-derived exosomes alleviated the II/R injury and promoted gut damage recovery via exosomal miR-23a-3p and its downstream target molecule-MAP4K4.

show abstract

Galactomannan as a Potential Modulator of Intestinal Ischemia–Reperfusion Injury

Abstract: Conclusions: GAL pretreatment constitutes a novel and promising therapy to reduce local and remote damage triggered by intestinal ischemiaereperfusion injury. Further in vivo and in vitro studies to understand GAL's modulatory effects are warranted.

Cited by 9 publications

References 26 publications

Induction of Endotoxin Tolerance Delays Acute Rejection in a Hindlimb Transplantation Model in Rats

Induction of Endotoxin Tolerance Delays Acute Rejection in a Hindlimb Transplantation Model in Rats

Diosgenin and galactomannans, natural products in the pharmaceutical sciences

Intestinal Epithelial Cell Derived Exosomes Package MicroRNA-23a-3p Alleviate Gut Damage After Ischemia/Reperfusion via Targeting MAP4K4

Contact Info

Product

Resources

About