Salidroside Attenuates Concanavalin A-Induced Hepatitis via Modulating Cytokines Secretion and Lymphocyte Migration in Mice

Abstract

Salidroside, isolated from the medicinal plant Rhodiola, was reported to serve as an “adaptogen.” This study was designed to explore the protective effect of salidroside on concanavalin A- (Con A-) induced hepatitis in mice and investigate potential mechanisms. C57BL/6 mice were randomly divided into control group, Con A group, and salidroside group. Salidroside (50 mg/kg) was injected intravenously followed by Con A administration. The levels of ALT, AST, inflammatory cytokines and CXCL-10 were examined. The pathological damage of livers was assessed, the amounts of phosphorylated IκBα and p65 were measured, and the numbers of CD4+ and CD8+ T lymphocytes in the blood, spleen and infiltrated in the liver were calculated. Our results showed that salidroside pretreatment reduced the levels of ALT, AST dramatically and suppressed the secretion of proinflammatory cytokines through downregulating the activity of NF-κB partly. Salidroside altered the distribution of CD4+ and CD8+ T lymphocyte in the liver and spleen through regulating CXCL-10 and decreased the severity of liver injuries. In conclusion, these results confirm the efficacy of salidroside in the prevention of immune mediated hepatitis in mice.

Phenylethanoid Glycosides: Research Advances in Their Phytochemistry, Pharmacological Activity and Pharmacokinetics

“…injection of 123 dramatically reduced the levels of alanine aminotransferase and aspartic transaminase in the above mentioned mouse model, and partly suppressed the secretion of proinflammatory cytokines through downregulating the activity of NF-κB. Meanwhile, compound 123 altered the distribution of CD4 + and CD8 + T lymphocyte in the liver and spleen through regulating CXCL-10 and decreased the severity of liver injuries [99]. Song extracted TPG from L. purpurascens and tested the immune enhancement effect of the TPG using serum hemolysin antibody, phagocytosis, splenocyte antibody production, and NK cells activity assays.…”

Comparison of Concanavalin a-Induced Murine Autoimmune Hepatitis Models

“…Liver samples were fixed in 4% buffered paraformaldehyde for 48 h. Sections (4-5 µm) on slides were deparaffinized with xylene, rehydrated with decreasing concentrations of ethanol, and stained with hematoxylin and eosin (H&E). Then, all sections were graded blindly under a light microscope according to the following criteria: 0, none; 1, individual cell necrosis; 2, ≤30% lobular necrosis; 3, ≤60% lobular necrosis; and 4, > 60% lobular necrosis [9]. …”

“…AIH is a worldwide health problem and a significant cause of mortality; it has been estimated that AIH has an annual incidence of approximately 2 in 100, 000 individuals and a prevalence of 15 cases per 100, 000 persons worldwide [8]. Without treatment, nearly 50% of patients with severe AIH die in approximately 5 years [9, 10]. The incidence rate is also different between men and women.…”

Morphological Changes in Mice Liver in Dynamics of Concanavalin a - Induced Hepatitis

“…Найважливішим ланцюгом при Кон А-гепатиті є активація Т-клітин, в тому числі печінкових лімфоцитів-кіллерів, а також взаємодія Т-хелперів і макрофагів [1,4,5]. Однак серед чисельних літературних даних патоморфологічні особливості дії лек-тину на печінку описані поверхнево [6][7][8]. Ці фрагментарні відомості не дають повної уяви щодо динаміки процесів, котрі відбуваються при експериментальному гепатиті.…”

“…На тлі ранніх судинних запаль-них проявів у печінці реєструвалося істотне збільшення кількості клітин природного та адаптивного імунітету. Інфільтрація тканини печінки лейкоцитами є характерною морфо-логічною рисою аутоімунних захворювань органа [1,3,6,15]. Вважають, що, іммунноопо-середковане пошкодження підтримується по-вторюваними циклами безперервної міграції, утримання, виживання і загибелі ефекторних лейкоцитів [9,17].…”