Synergic Anti-Pruritic and Anti-Inflammatory Effects of Scutellariae Radix plus Flos Loncerae Extracts in Rat Peritoneal Mast Cell and Chemical Antigen-Induced Mice

2015 ◽  
Vol 7 (4s) ◽  
pp. 470-479 ◽  
Author(s):  
Saurabh Gupta ◽  
Satish Kumar Muthureddy Nataraj ◽  
K. Rama Satyanarayana Raju ◽  
Shashank Mulukutla ◽  
Nilesh Ambore ◽  
...  

1963 ◽  
Vol 41 (1) ◽  
pp. 1901-1906
Author(s):  
Frank C. Monkhouse ◽  
Donald G. Baker

Experiments were carried out to determine whether changes in endogenous heparin in rat tissues were related to changes in plasma levels of clearing factor lipase (CFL). Skin heparin levels, postheparin plasma CFL levels, and peritoneal mast cell counts were measured in normal, adrenalectomized, cortisone-treated, and X-irradiated rats. Total body X-irradiation in doses of 400 r to 600 r decreased skin heparin levels. The postheparin CFL levels of irradiated rats remained high while that of pair-fed controls dropped significantly. Cortisone treatment for 6 days caused an increase in plasma CFL levels in both intact and adrenalectomized rats but no significant change in skin heparin levels or mast cell count. Adrenalectomy caused no significant change in either postheparin CFL or skin heparin levels.


2013 ◽  
Vol 45 (1) ◽  
pp. 83 ◽  
Author(s):  
Saurabh Gupta ◽  
B Duraiswamy ◽  
MN Satishkumar

2019 ◽  
Vol 20 (20) ◽  
pp. 5025 ◽  
Author(s):  
Ewelina Russjan ◽  
Katarzyna Kaczyńska

Neurotensin (NT) demonstrates ambiguous activity on inflammatory processes. The present study was undertaken to test the potential anti-inflammatory activity of NT in a murine model of non-atopic asthma and to establish the contribution of NTR1 receptors. Asthma was induced in BALB/c mice by skin sensitization with dinitrofluorobenzene followed by intratracheal hapten provocation. The mice were treated intraperitoneally with NT, SR 142948 (NTR1 receptor antagonist) + NT or NaCl. Twenty-four hours after the challenge, airway responsiveness to nebulized methacholine was measured. Bronchoalveolar lavage fluid (BALF) and lungs were collected for biochemical and immunohistological analysis. NT alleviated airway hyperreactivity and reduced the number of inflammatory cells in BALF. These beneficial effects were inhibited by pretreatment with the NTR1 antagonist. Additionally, NT reduced levels of IL-13 and TNF-α in BALF and IL-17A, IL12p40, RANTES, mouse mast cell protease and malondialdehyde in lung homogenates. SR 142948 reverted only a post-NT TNF-α decrease. NT exhibited anti-inflammatory activity in the hapten-induced asthma. Reduced leukocyte accumulation and airway hyperresponsiveness indicate that this beneficial NT action is mediated through NTR1 receptors. A lack of effect by the NTR1 blockade on mast cell activation, oxidative stress marker and pro-inflammatory cytokine production suggests that other pathways can be involved, which requires further research.


Cephalalgia ◽  
2012 ◽  
Vol 32 (4) ◽  
pp. 337-345 ◽  
Author(s):  
Michael Baun ◽  
Martin Holst Friborg Pedersen ◽  
Jes Olesen ◽  
Inger Jansen-Olesen

Background: Pituitary adenylate cyclase activating peptide-38 (PACAP-38) has been shown to induce migraine in migraineurs, whereas the related peptide vasoactive intestinal peptide (VIP) does not. In the present study we examine the hypothesis that PACAP-38 and its truncated version PACAP-27 but not VIP cause degranulation of mast cells in peritoneum and in dura mater. Methods: The degranulatory effects of PACAP-38, PACAP-27 and VIP were investigated by measuring the amount of N-acetyl-β-hexosaminidase released from isolated peritoneal mast cells and from dura mater attached to the skull of the rat in vitro. In peritoneal mast cells N-truncated fragments of PACAP-38 (PACAP(6–38), PACAP(16–38) and PACAP(28–38)) were also studied. To investigate transduction pathways involved in mast cell degranulation induced by PACAP-38, PACAP-27 and VIP, the phospholipase C inhibitor U-73122 and the adenylate cyclase inhibitor SQ 22536 were used. Results: The peptides induced degranulation of isolated peritoneal mast cells of the rat with the following order of potency: PACAP-38 = PACAP(6–38) = PACAP(16–38) » PACAP-27 = VIP = PACAP(28–38). In the dura mater we found that 10−5 M PACAP-38 was significantly more potent in inducing mast cell degranulation than the same concentration of PACAP-27 or VIP. Inhibition of intracellular mechanisms demonstrated that PACAP-38-induced degranulation is mediated by the phospholipase C pathway. Selective blockade of the PAC1 receptor did not attenuate degranulation. Conclusion: These findings correlate with clinical studies and support the hypothesis that mast cell degranulation is involved in PACAP-induced migraine. PACAP-38 has a much stronger degranulatory effect on rat peritoneal and dural mast cells than VIP and PACAP-27. The difference in potency between PACAP-38- and PACAP-27/VIP-induced peritoneal mast cell degranulation is probably not related to the PAC1 receptor but is caused by a difference in efficacy on phospholipase C.


1992 ◽  
Vol 26 (3) ◽  
pp. 293-303 ◽  
Author(s):  
Meir Shalit ◽  
Naomi Riesel-Yaron ◽  
Francesca Levi-Schaffer

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