Magnolol Attenuates the Lung Injury in Hypertonic Saline Treatment from Mesenteric Ischemia Reperfusion through Diminishing iNOS

Shih, Hsin-Chin; Huang, Mu-Shun; Lee, Chen‐Hsen

doi:10.1016/j.jss.2011.04.063

Cited by 10 publications

(2 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…15, 28 During the disease progression, complement is activated producing complement components such as C3a and C5a. 20, 29, 30 Complement cascades are necessary for the initiation and amplification of tissue injury.…”

Section: Discussionmentioning

confidence: 99%

Complement C5a exacerbates acute lung injury induced through autophagy-mediated alveolar macrophage apoptosis

Jiang

et al. 2014

Cell Death Dis

View full text Add to dashboard Cite

Intestinal ischemia has a high mortality and often causes acute lung injury (ALI), which is a serious complication, and is accompanied by high mortality up to 40%. An intense local and systemic inflammation occurs during intestinal ischemia/reperfusion (IR)-induced lung injury resulting from activation of immune responses. It has been reported that one component of complement, C5a, is indispensable for the full development of IR-induced lung injury, whereas the detailed molecular mechanism remains to be elucidated. In this study, we found that intestinal IR induced ALI-like symptoms, and C5a receptor (C5aR) expression was upregulated in alveolar macrophages, which are resident macrophages in lung tissue and are important in pulmonary homeostasis. C5a produced during lung injury binds to C5aR in alveolar macrophages, initiates downstream signaling that promotes autophagy, leading to apoptosis of alveolar macrophages. Using Mφ-ATG5−/− mice, in which the atg5 is deficient specifically in macrophages and autophagy is inhibited, we confirmed that in vivo C5a interacting with C5aR induced autophagy in alveolar macrophages, which promoted alveolar macrophage apoptosis. Further study indicated that autophagy was induced through C5aR-mediated degradation of bcl-2. Taken together, our results demonstrated that C5aR-mediated autophagy induced apoptosis in alveolar macrophages, disrupting pulmonary homeostasis and contributing to the development of ALI. This novel mechanism suggests new therapeutic potential of autophagy regulation in ALI.

show abstract

Section: Discussionmentioning

confidence: 99%

Complement C5a exacerbates acute lung injury induced through autophagy-mediated alveolar macrophage apoptosis

Jiang

et al. 2014

Cell Death Dis

View full text Add to dashboard Cite

show abstract

“…Intestinal I/R can initiate a cascade of physiological processes resulting in remote injury to organs including the lungs , liver , and kidneys . The lungs are particularly vulnerable, due to the exposure of their extensive capillary bed to post‐ischemia blood, which contains reactive oxygen species , mast cells , leukocytes , and inflammatory mediators . If left untreated, intestinal I/R injury subsequently results in MODS and MOF .…”

Section: Discussionmentioning

confidence: 99%

Monitoring dynamic alterations in calcium homeostasis by T₁‐mapping manganese‐enhanced MRI (MEMRI) in the early stage of small intestinal ischemia–reperfusion injury

et al. 2015

View full text Add to dashboard Cite

Manganese-enhanced MRI studies have proven to be useful in monitoring physiological activities associated with calcium ions (Ca(2+)) due to the paramagnetic property of the manganese ion (Mn(2+)), which makes it an excellent probe of Ca(2+) . In this study, we developed a method in which a Mn(2+)-enhanced T1 -map MRI could enable the monitoring of Ca(2+) influx during the early stages of intestinal ischemia-reperfusion (I/R) injury. The Mn(2+) infusion protocol was optimized by obtaining dose-dependent and time-course wash-out curves using a Mn(2+)-enhanced T1-map MRI of rabbit abdomens following an intravenous infusion of 50 mmol/l MnCl2 (5-10 nmol/g body weight (BW)). In the rabbit model of intestinal I/R injury, T1 values were derived from the T1 maps in the intestinal wall region and revealed a relationship between the dose of the infused MnCl2 and the intestinal wall relaxation time. Significant Mn(2+) clearance was also observed over time in control animals after the infusion of Mn(2+) at a dose of 10 nmol/g BW. This technique was also shown to be sensitive enough to monitor variations in calcium ion homeostasis in vivo after small intestinal I/R injury. The T1 values of the intestinal I/R group were significantly lower (P < 0.05) than that of the control group at 5, 10, and 15 min after Mn(2+) infusion. Our data suggest that MnCl2 has the potential to be an MRI contrast agent that can be effectively used to monitor changes in intracellular Ca(2+) homeostasis during the early stages of intestinal I/R injury.

show abstract

Effects and Mechanism Analysis of Combined Infusion by Levosimendan and Vasopressin on Acute Lung Injury in Rats Septic Shock

Wang

Liu

et al. 2014

Cell Biochem Biophys

View full text Add to dashboard Cite

This research is aimed to discover the influence and underling mechanism of combined infusion of arginine vasopressin with levosimendan on acute lung injury in rat septic shock with norepinephrine supplemented. The traditional fecal peritonitis-induced septic shock model was undergone in rats for study. It is observed that the combined infusion supplemented with norepinephrine brought about a lower mean pulmonary artery pressure; lower high-mobility group box 1 levels, pulmonary levels of interleukin-6, and arterial total nitrate/nitrite; lower apoptotic cells scores and total histological scores; but higher pulmonary gas exchange when compared with the separate infusion group and norepinephrine group. This therapy shows potential clinical beneficial assistance in sepsis-induced acute lung injury. The results suggest the mechanism of such effect is through abating pulmonary artery pressure, and more importantly suppressing inflammatory responses in lung when compared with norepinephrine infusion group and the separate infusion of levosimendan or vasopressin alone.

show abstract

Magnolol Attenuates the Lung Injury in Hypertonic Saline Treatment from Mesenteric Ischemia Reperfusion through Diminishing iNOS

Cited by 10 publications

References 28 publications

Complement C5a exacerbates acute lung injury induced through autophagy-mediated alveolar macrophage apoptosis

Complement C5a exacerbates acute lung injury induced through autophagy-mediated alveolar macrophage apoptosis

Monitoring dynamic alterations in calcium homeostasis by T₁‐mapping manganese‐enhanced MRI (MEMRI) in the early stage of small intestinal ischemia–reperfusion injury

Effects and Mechanism Analysis of Combined Infusion by Levosimendan and Vasopressin on Acute Lung Injury in Rats Septic Shock

Contact Info

Product

Resources

About

Magnolol Attenuates the Lung Injury in Hypertonic Saline Treatment from Mesenteric Ischemia Reperfusion through Diminishing iNOS

Cited by 10 publications

References 28 publications

Complement C5a exacerbates acute lung injury induced through autophagy-mediated alveolar macrophage apoptosis

Complement C5a exacerbates acute lung injury induced through autophagy-mediated alveolar macrophage apoptosis

Monitoring dynamic alterations in calcium homeostasis by T1‐mapping manganese‐enhanced MRI (MEMRI) in the early stage of small intestinal ischemia–reperfusion injury

Effects and Mechanism Analysis of Combined Infusion by Levosimendan and Vasopressin on Acute Lung Injury in Rats Septic Shock

Contact Info

Product

Resources

About

Monitoring dynamic alterations in calcium homeostasis by T₁‐mapping manganese‐enhanced MRI (MEMRI) in the early stage of small intestinal ischemia–reperfusion injury