Biology subjects

Woo, D.-C.

Publications and source records attributed to Woo, D.-C..

2 recordsLinked to original sources

bioRxiv2024

Impact of Cervical Lymphatic Obstruction on Brain Pathophysiology in Cervical Lymphedema Animal Models

BackgroundInjury to the cervical lymph nodes can lead to cervical lymphedema and subsequent fluid accumulation in the head and neck region, potentially causing pathophysiological alteration in the brain. This condition is thought to be linked with various neurological diseases, although the direct connection between cervical lymphatic obstruction and its effect on the brain has been difficult to establish. MethodsWe produced the disease animal models through lymph node dissection and radiation in fifteen male Sprague-Dawley rats aged 8 weeks and weighing 280-320 g. The models were specifically designed to induce lymphatic obstruction in the cervical region only, with no direct interventions applied to the brain. We evaluated swelling and lymphatic drainage in the head and neck for follow-up. The size of the lateral ventricles was verified through MRI, and changes in water content in brain tissue were directly measured. At 2 and 8 weeks, we observed immune cell infiltration, ventricular enlargement, and pathohistological changes in the harvested brain tissues. ResultsThe experimental animals exhibited lymphatic obstruction in the cervical region, with swelling, abnormal lymphatic drainage, and immune cell infiltration into the brains white matter, reminiscent of extremities lymphedema. MRI revealed lateral ventricular enlargement in these animals, indicative of increased cerebrospinal fluid levels compared to the control group. This increase in cerebrospinal fluid was associated with an increase in brain tissue water content, leading to pathophysiological changes akin to those seen in hydrocephalus and cerebral edema. ConclusionThe outcomes in this study underscore a significant link between lymphatic circulatory dysfunction and the onset of neurophysiological diseases. Cervical lymphedema showed pathophysiological changes similar to those seen in extremities lymphedema. However, these changes in the brain could be more critical than in the extremities. Our finding highlights the importance of understanding lymphatic system health in preventing and managing neurological conditions.

physiology↗

bioRxiv2019

6-O-galloylsalidroside, an active ingredient from Acer tegmentosum, ameliorates alcoholic steatosis and liver injury in a mouse model of chronic ethanol consumption

We previously reported that Acer tegmentosum extract, which is traditionally used to treat liver disease in Korea, may help reduce fat accumulation, improve liver metabolism, and suppress inflammation in alcoholic liver disease. The active ingredient was found to be 6-O-galloylsalidroside, which was isolated from the methanol extract of A. tegmentosum. We hypothesized that 6-O-galloylsalidroside extracted from A. tegmentosum may help protect from liver damage and attenuate hepatic fat accumulation associated with chronic alcohol consumption. In the present study, we aimed to investigate whether 6-O-galloylsalidroside can regulate alcoholic fatty liver and liver injury in mice. For this purpose, mice were fed with Lieber-DeCarli 5% ethanol diet for 11 days to induce steatosis and liver injury. Oral 6-O-galloylsalidroside was administered once a day for 11 days. Intrahepatic lipid accumulation caused by alcohol consumption was measured using in vivo 1H magnetic resonance imaging. Hepatic steatosis was observed histologically in tissue samples stained with hematoxylin and eosin, as well as Oil Red O. The serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured, as well as the triglyceride content in liver homogenates. On magnetic resonance spectroscopy, 6-O-galloylsalidroside appeared to alleviate alcohol-induced steatosis, which was reflected in decreased hepatic and serum triglyceride levels despite ethanol feeding. Furthermore, 6-O-galloylsalidroside treatment was associated with decreased RNA expression of Cd36, which plays an important role in the development of alcoholic steatosis through the hepatic de novo lipogenesis pathway. Furthermore, treatment with 6-O-galloylsalidroside inhibited the expression of cytochrome P4502E1 and attenuated hepatocellular damage, reflected in reduced ALT and AST levels. These findings suggest that 6-O-galloylsalidroside extracted from A. tegmentosum might serve as a bioactive agent for treating alcoholic fatty liver and liver damage.

biochemistry↗