scholarly journals Evaluation of the possible apitherapeutic value of bee venom and bee propolis on L-arginine-induced acute pancreatitis and lung injury in albino rats

2020 ◽  
Vol 5 (1) ◽  
pp. 1-12
Author(s):  
Noha Abd El Latif Ibrahim ◽  
Sahar Bastawy Ahmed ◽  
Aliaa Ali Hassan ◽  
Nehad Ahmed Sadek ◽  
Maha Khaled Abdelwahed
2001 ◽  
Vol 280 (5) ◽  
pp. G974-G978 ◽  
Author(s):  
Madhav Bhatia ◽  
Ashok K. Saluja ◽  
Vijay P. Singh ◽  
Jean-Louis Frossard ◽  
Hong-Sik Lee ◽  
...  

Complement factor C5a acting via C5a receptors (C5aR) is recognized as an anaphylotoxin and chemoattractant that exerts proinflammatory effects in many pathological states. The effects of C5a and C5aR in acute pancreatitis and in pancreatitis-associated lung injury were evaluated using genetically altered mice that either lack C5aR or do not express C5. Pancreatitis was induced by administration of 12 hourly injections of cerulein (50 μg/kg ip). The severity of pancreatitis was determined by measuring serum amylase, neutrophil sequestration in the pancreas, and acinar cell necrosis. The severity of lung injury was evaluated by measuring neutrophil sequestration in the lung and pulmonary microvascular permeability. In both strains of genetically altered mice, the severity of pancreatitis and pancreatitis-associated lung injury was greater than that noted in the comparison wild-type strains of C5aR- and C5-sufficient animals. This exacerbation of injury in the absence of C5a function indicates that, in pancreatitis, C5a exerts an anti-inflammatory effect. Potentially, C5a and its receptor are capable of both promoting and reducing the extent of acute inflammation.


2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Qiang Fu ◽  
Zhensheng Zhai ◽  
Yuzhu Wang ◽  
Lixia Xu ◽  
Pengchong Jia ◽  
...  

The rapid production and release of a large number of inflammatory cytokines can cause excessive local and systemic inflammation in severe acute pancreatitis (SAP) and multiple organ dysfunction syndrome (MODS), especially pancreatitis-associated acute lung injury (P-ALI), which is the main cause of early death in patients with SAP. The NLRP3 inflammasome plays an important role in the maturation of IL-1β and the inflammatory cascade. Here, we established a model of SAP using wild-type (NLRP3+/+) and NLRP3 knockout (NLRP3-/-) mice by intraperitoneal injections of caerulein (Cae) and lipopolysaccharide (LPS). Pathological injury to the pancreas and lungs, the inflammatory response, and neutrophil infiltration were significantly mitigated in NLRP3-/- mice. Furthermore, INF-39, an NLRP3 inflammasome inhibitor, could reduce the severity of SAP and P-ALI in a dose-dependent manner. Our results suggested that SAP and P-ALI were alleviated by NLRP3 deficiency in mice, and thus, reducing NLRP3 expression may mitigate SAP-associated inflammation and P-ALI.


2017 ◽  
Vol 213 (11) ◽  
pp. 1370-1377 ◽  
Author(s):  
Liang Zhao ◽  
Teng Zuo ◽  
Qiao Shi ◽  
Fang-chao Mei ◽  
Yu-pu Hong ◽  
...  

2003 ◽  
Vol 83 (4) ◽  
pp. 471-478 ◽  
Author(s):  
Catherine M Pastor ◽  
Laura Rubbia-Brandt ◽  
Antoine Hadengue ◽  
Martha Jordan ◽  
Philippe Morel ◽  
...  

Gut ◽  
2009 ◽  
Vol 58 (6) ◽  
pp. 813-819 ◽  
Author(s):  
R Sharif ◽  
R Dawra ◽  
K Wasiluk ◽  
P Phillips ◽  
V Dudeja ◽  
...  

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