ABSTRACT
Gynura root has been used extensively in Chinese folk medicine and plays a role in promoting microcirculation and relieving pain. However, its hepatic toxicity should not be neglected. Recently, we admitted a 62-year old female who developed hepatic veno-occlusive disease (HVOD) after ingestion of Gynura root. Only a few articles on HVOD induced by Gynura root have been reported in the literature. It is suspected that pyrrolizidine alkaloids in Gynura root might be responsible for HVOD. In this paper, we report a case of HVOD and review the literature.
Subject(s)
Asteraceae/adverse effects , Drugs, Chinese Herbal/adverse effects , Hepatic Veno-Occlusive Disease/etiology , Phytotherapy/adverse effects , Plant Roots/adverse effects , Drugs, Chinese Herbal/therapeutic use , Female , Hepatic Veno-Occlusive Disease/diagnosis , Humans , Middle Aged , Neck Pain/drug therapyABSTRACT
OBJECTIVE: To explore the effect of muscovite on the quality of gastric ulcer healing. METHOD: Gastric ulcers were produced in male rats by serosal application of acetic acid. Rats were gavaged for 14 days with saline, omeprazole and muscovite starting 3 days after ulcer induction. Then the tissue and blood samples were obtained and measured. RESULT: In the muscovite group, restored mucosa thickness increased, cystically dilated glands decreased, microvessels in connective tissue increased, the secretion of mucus, hexosamine, PGE2, EGF, bFGF were enhanced, and the express of EGFR was stronger. CONCLUSION: Muscovite can promote the gastric ulcer healing and improve the quality of gastric ulcer healing.
Subject(s)
Aluminum Silicates/pharmacology , ErbB Receptors/metabolism , Materia Medica/pharmacology , Stomach Ulcer/pathology , Animals , Dinoprostone/blood , Fibroblast Growth Factor 2/metabolism , Gastric Mucosa/pathology , Gastric Mucosa/physiopathology , Hexosamines/metabolism , Male , Mucus/metabolism , Rats , Rats, Wistar , Stomach Ulcer/chemically induced , Stomach Ulcer/physiopathologyABSTRACT
OBJECTIVE: To investigate the mechanism of isinglass in the prevention and treatment of chronic atrophic gastritis (CAG) in rats. METHOD: Animal models of SD rats with CAG were made in accordance with the previous experience of combined administration of 60% ethanol, 20 mmol x L(-1) sodium deoxycholate and 0.1% ammonia water. In prevention groups, sucralfate and isinglass were used as preventive therapy while CAG rat model was being made. In the reverse groups, sucralfate and isinglass were used to treat rats after establishment of CAG rat model. Finally all the rats were executed. Then the length of the proliferation zone of the gastric mucosa and serum epidermal growth factors (EGF) and growth hormones (GH)level were studied. RESULT: In isinglass prevention groups and high dose isinglass reverse group, the length of the proliferation zone of the gastric mucosa was very close to that in normal control group (P > 0.05), much better than model control group (P < 0.01). In low dose isinglass reverse group, it was lower than that in normal control group (P < 0.01), but much better than model control group (P < 0.01). In both prevention and reverse groups, serum EGF level was higher than that in normal (P < 0.01) and model control group (P < 0.05). Serum GH level was the same in every group (P > 0.05). CONCLUSION: The mechanism of isinglass in the prevention and treatment of CAG rats lies in revitalizing and proliferating gastric mucosal cells by stimulating endogenous EGF secretion.
Subject(s)
Gastritis, Atrophic , Gelatin/therapeutic use , Materia Medica/therapeutic use , Animals , Chronic Disease , Dose-Response Relationship, Drug , Epidermal Growth Factor/blood , Female , Gastritis, Atrophic/chemically induced , Gastritis, Atrophic/drug therapy , Gastritis, Atrophic/prevention & control , Gelatin/administration & dosage , Growth Hormone/blood , Materia Medica/administration & dosage , Proliferating Cell Nuclear Antigen/metabolism , Rats , Rats, Sprague-DawleyABSTRACT
OBJECTIVE: To evaluate the effect of isinglass on the prevention and treatment of chronic atrophic gastritis in rats. METHOD: Animal model of SD rats with CAG was established in accordance with the previous experience of combined administration of 60% ethanol, 20 mmol x L(-1) sodium deoxycholate and 0.1% ammonia water. In prevention groups, sucralfate and isinglass were used as preventive therapy while we were establishing CAG rat model. In the reverse groups, sucralfate and isinglass were used to treat rats after establishment of CAG rat model. Finally all the rats were executed and pathologic changes of the gastric mucosa were studied by gross appearance and microscopy. RESULT: In isinglass prevention groups and reverse groups, inflammation grades of gastric antrum were less than these in model control group (P < 0.01) while the means of ratios of the thickness of gastric mucosal gland and muscularis mucos (L1/L2), the number of gastric glands in 1-mm lengths of mucosal layer were much better than those in model control group (P < 0.01). They were very close to normal control group (P > 0.05). CONCLUSION: Isinglass can prevent the gastric mucosal atrophy in the CAG model and can improve and cure the gastric mucosal atrophy of the SD rats with GAG.