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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.
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http://dx.doi.org/10.1002/nbm.3335 | DOI Listing |
Histol Histopathol
September 2025
Department of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, China.
Brazilin, a natural homoisoflavonoid, is the primary bioactive ingredient derived from the bark and heartwood of L. It has been proven to exhibit multiple biological activities and therapeutic potential in chronic degenerative diseases, fibrotic disorders, inflammatory diseases, and cancers. However, whether it is involved in regulating the pathological process of acute kidney injury (AKI) is not fully understood.
View Article and Find Full Text PDFJ Mol Histol
September 2025
Hebei Medical University, No. 361, Zhongshan East Road, Shijiazhuang, 050017, China.
Numerous people experiencing acute myocardial infarction are also experiencing myocardial ischemia-reperfusion injury (MIRI). Pyroptosis is a core mechanism in MIRI. Tongxinluo (TXL) has a significant protective effect on endothelial cell function.
View Article and Find Full Text PDFJ Ethnopharmacol
September 2025
Department of Traditional Chinese Medicine, Qingdao Municipal Hospital, Qingdao, China. Electronic address:
Ethnopharmacological Relevance: Acute kidney injury (AKI) is a growing worldwide health concern. Danggui Shaoyao San (DGSYS) was an frequently-used representative prescription to "promote blood and water and harmonize the body" in traditional Chinese medicine, and its underlying mechanism against AKI remains to be elucidated.
Aim Of The Study: To investigate the protective effect and potential molecular mechanism of DGSYS in alleviating AKI by network pharmacology and experiment validation.
Eur J Pharmacol
September 2025
Department of Cardiovascular Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, China. Electronic address:
Purpose: Ischemia-reperfusion injury remains a major problem following myocardial infarction. Alpinetin (ALPT) has been reported to exhibit cardioprotective effects as well as resistance to ischemia-reperfusion injury. However, its role and mechanism during myocardial ischemia-reperfusion injury are unknown.
View Article and Find Full Text PDFFree Radic Biol Med
September 2025
Laboratory of Clinical and Experimental Pathology, Xuzhou Medical University, Xuzhou, China; National Demonstration Center for Experimental Basic Medical Science Education, Xuzhou Medical University, Xuzhou China. Electronic address:
Elevated H3K27me3 levels during cerebral I/R injury exacerbate neuronal damage through oxidative stress, but the underlying mechanism remains to be elucidated. We hypothesized that reduced H3K27me3 confers protection by modulating FOXP1 expression. Employing multifaceted approaches, we demonstrate that H3K27me3 reduction in vivo and in vitro enhances lipid metabolism and rescues oxygen-glucose deprivation (OGD)-induced mitochondrial morphological abnormalities and functional deficits.
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