[Advance in studies on anti-inflammatory effect of Uygur medicine].
Liu Yan,Zhang Li,Huang Hua
Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
Inflammation refers to the defensive reaction of living organisms with vascular systems against damage factors, and gets involved in the pathogenesis of many diseases. Uygur medicine is an important component of traditional Chinese medicine, as well as one of the four major ethnic medicines. It is widely applied in the clinical treatment of inflammatory diseases. In recent years, many domestic and foreign scholars have studied the anti-inflammatory effect and mechanism of effective components, effective fractions, extracts and compound preparations of Uygur medicine. In this paper, the authors summarized anti-inflammatory Uygur medicine, in the expectation of providing reference for discovering new anti-inflammatory drugs from Uygur medicine.
Amelioration by chicory seed extract of diabetes- and oleic acid-induced non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) via modulation of PPARα and SREBP-1.
Ziamajidi Nasrin,Khaghani Shahnaz,Hassanzadeh Gholamreza,Vardasbi Safura,Ahmadian Shahram,Nowrouzi Azin,Ghaffari Seyed Mahmood,Abdirad Afshin
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
We evaluated the effect of chicory (Cichorium intybus L.) seed extract (CI) on hepatic steatosis caused by early and late stage diabetes in rats (in vivo), and induced in HepG2 cells (in vitro) by BSA-oleic acid complex (OA). Different dosages of CI (1.25, 2.5 and 5 mg/ml) were applied along with OA (1 mM) to HepG2 cells, simultaneously and non-simultaneously; and without OA to ordinary non-steatotic cells. Cellular lipid accumulation and glycerol release, and hepatic triglyceride (TG) content were measured. The expression levels of sterol regulatory element-binding protein-1c (SREBP-1c) and peroxisome proliferator-activated receptor alpha (PPARα) were determined. Liver samples were stained with hematoxylin and eosin (H&E). Significant histological damage (steatosis-inflammation-fibrosis) to the cells and tissues and down-regulation of SREBP-1c and PPARα genes that followed steatosis induction were prevented by CI in simultaneous treatment. In non-simultaneous treatment, CI up-regulated the expression of both genes and restored the normal levels of the corresponding proteins; with a greater stimulating effect on PPARα, CI acted as a PPARα agonist. CI released glycerol from HepG2 cells, and targeted the first and the second hit phases of hepatic steatosis. A preliminary attempt to characterize CI showed caffeic acid, chlorogenic acid, and chicoric acid, among the constituents.
Effect of Cichorium intybus L. on the expression of hepatic NF-κB and IKKβ and serum TNF-α in STZ- and STZ+ niacinamide-induced diabetes in rats.
Rezagholizadeh Lotfollah,Pourfarjam Yasin,Nowrouzi Azin,Nakhjavani Manuchehr,Meysamie Alipasha,Ziamajidi Nasrin,Nowrouzi Peyman S
Diabetology & metabolic syndrome
BACKGROUND:Inflammation is an early event in the development of diabetes type 2 (T2D). Cichorium intybus L. (chicory) possesses anti-inflammatory action. We compared the anti-inflammatory aspect of aqueous chicory seed extract (CSE) in early and late stage T2D in rats. METHODS:Wistar albino rats were divided into nine final groups (n = 6). Three main groups consisted of non-diabetic (Control), early stage diabetes (ET2D; niacinamide/streptozotocin, i.e., NIA/STZ), and late stage diabetes (LT2D; STZ). Within each main group, a subgroup was treated with CSE (125 mg/kg; i.p.); within each diabetic group (STZ and NIA/STZ) a subgroup received metformin (100 mg/kg; i.p.); another subgroup in STZ group received aspirin (120 mg/kg; oral). After 21 days, fasting blood glucose (FBS), insulin, and TNF-α level were measured in serum; IKKβ and NF-κB (p65) mRNA and protein expression were evaluated by real time PCR and Western blotting; p65 DNA binding activity was determined by ELISA, in liver tissue. RESULTS:The mRNA and protein expression levels of IKKβ, and P65 genes increased in both stages of T2D (p < 0.01); CSE decreased their expression (p < 0.001, mRNAs; p < 0.05, proteins). The increased DNA-binding capacity of NF-κB (p < 0.0001) in diabetes was lowered by CSE (p < 0.001). The effect of CSE was limited to ET2D requiring insulin. CONCLUSIONS:The anti-inflammatory action of CSE is due to a direct modulation of cytokine expression. The dependency of chicory action on the presence of insulin indicates its usefulness in the early stages of diabetes and for the purpose of preventing and delaying diabetes onset.