This study was carried out to investigate the protective effect of prednisolone in rabbit primary cultured articular chondrocytes treated with sodium nitroprusside (SNP), a nitric oxide donor. After a cell phenotype was determined, the MTT assay and Western blot analysis of type II collagen, cylooxygenase-2 (COX-2) and phosphorylated extracellular regulated kinase (pERK) were performed in the control, SNP (298 μg/ml) alone or SNP plus prednisolone (0.05-50 μg/ml)-treated rabbit articular chondrocytes. Immunofluorescence staining of type II collagen was also performed. Cell morphology indicated that SNP treatment induced cytotoxicity, and that the SNP-induced cytotoxicity was inhibited by prednisolone treatment. MTT assay showed that the SNP treatment resulted in a significant decrease in the level of cell viability compared with that of control (p<0.01), and that the prednisolone treatment resulted in a decrease in the SNP-induced cytotoxicity. SNP treatment resulted in a decrease in the level of type II collagen, compared with the control chondrocytes. The prednisolone treatment recovered the down-regulated expression of type II collagen induced by SNP, showing a significant level in 5 μg/ml of the prednisolone treatment group compared to the SNP treatment group (p<0.05). A significant increase in COX-2 was significantly induced by the SNP treatment compared to control chondrocytes (p<0.01). The COX-2 expression was decreased by the prednisolone treatment, showing a significant level in 50 μg/ml of the prednisolone treatment group compared to the SNP treatment group (p<0.05). These phenomena was confirmed by immunofluorescence staining. Furthermore, the SNP treatment significantly induced a decrease of pERK expression compared to the control chondrocytes (p<0.01). The prednisolone treatment recovered its expression, showing a significant level in 0.5 μg/ml of the prednisolone treatment group compared to the SNP treatment group (p<0.05). Taken the above results together, prednisolone is considered to inhibit SNP-induced cell death and dedifferentiation, and modulated expression of COX-2 and pERK in rabbit articular chondrocytes.

A saccular aneurysm is a localized, pouch arterial abnormality, Varous kinds of experimental saccular aneurysm models have been developed to treat aneurysms, and more effective ways to create aneurysm model is also needed. This study aims to compare aneurysm models induced by either porcine pancreatic elastase or papain from papaya latex. Eleven New Zealand white rabbits were divided into three treatment groups: normal saline (n=3), papain (n=4), and elastase (n=4). The right common carotid artery was selected as the aneurysmal site, and the respective substance was incubated for 20 minutes. No neurological signs occurred after operation. Hematoxylin-eosin (H&E) staining and modified elastic trichrome stain were performed 2 weeks after the procedure for pathological analysis. Histological findings for the control group showed normal vascular wall structure, normal elastic fiber, and no signs of inflammation. In samples of the papain group, the vascular walls were damaged and the endothelium was detached. Most of the elastic fibers were destructed. All samples of the papain group showed elastic fragmentation. In the elastase group, all samples showed severe inflammation and destruction of the vascular structure. There was also an elastase-induced sterile abscess. These findings indicate that elastase does not induce stable aneurysms at a dose of 1 mg because of excessive inflammation and destruction of the vascular structure. Elastase induces inflammation and apoptosis which results in the vascular wall to weaken before an aneurysm is formed. Papain at the dose of 1 mg, in contrast, seems to be a suitable candidate for enzymatic aneurysm models in the rabbit.

Earthworms have been employed in traditional oriental medicine for the treatment of neurological disorders, as anticonvulsants, analgesics, and sedatives. In fact, earthworms are currently used as a medicinal agent in China, South Korea, Japan, Taiwan and North Korea. However, both the species and the genus of the earthworms registered in the pharmacopoeia of each country are different. Neural injury is induced by oxidative stress, inflammation, and apoptosis. The role of various synthetic chemicals of earthworms as antioxidant and anti-inflammatory agents have been studied and earthworm extract and its components have been shown to protect nerve cells and restore nerve function in various preclinical neuronal damage models. We employed earthworm extracts to provide prevention and treatment strategies for many neurodegenerative disorders including Parkinson's disease, mild cognitive impairment, cerebral infarction, and peripheral nerve damage. In this study, we investigated the effects of earthworm extracts and its components to explore their prophylactic and therapeutic effects in various neuropathic models. We used earthworm resources to provide prevention and treatment strategies for many neurodegenerative disorders including Parkinson's disease, mild cognitive impairment, cerebral infarction, and peripheral nerve damage. We summarized the protective effects of both earthworms and their extracts on neuropathies. The current study identified some earthworm components to be used in treatment and prevention strategies for nerve disorders and could be helpful for the development of new therapies for intractable diseases.