ginsenoside-rd and Body-Weight

ginsenoside-rd has been researched along with Body-Weight* in 2 studies

Other Studies

2 other study(ies) available for ginsenoside-rd and Body-Weight

ArticleYear
[Major hypoglycemic ingredients of Panax notoginseng saponins for treating diabetes].
    Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 2014, Volume: 45, Issue:2

    To explore the mechanism of Panax notoginseng saponins (PNS) on diabetes treatment and mass loss in KK-Ay mice with genetic type 2 diabetes mellitus (DM), and to identify the main hypoglycemic ingredients.. C57 and KK-Ay DM mice were divided into eight groups each comprising six mice: healthy normal, DM model, and DM model treated with PNS (200 mg/kg body mass), ginsenoside Re (Re, 14 mg/kg body mass), ginsenoside Rd (Rd, 15 mg/kg body mass), ginsenoside Rgl (Rg1, 40 mg/kg body mass), ginsenoside Rb1 (Rb1, 60 mg/kg body mass) and notoginsenoside R1 (R1, 6 mg/kg body mass). The PNS were intraperitoneal injection administered for 30 d, while the Re, RB1, Rg1, Rd and Re were intraperitoneal injection administered for 12 d. The fasting blood sugar (FBG), glucose tolerance (GT), serum insulin, leptin, body weight, food consumption, and levels of adipose tissue and blood lipid were determined.. On 12 d, lower FBG levels were found in the PNS and Rb1 treated mice compared with the model mice (P < 0.05). No statistical differences in FBG levels were found between the rest of the treatment groups and the model group (P > 0.05). After 30 d continuous administration of PNS, the FBG level of the mice further declined (P < 0.01). Meanwhile, the serum insulin (P < 0.05) and insulin resistance index (P < 0.01) of the PNS treated mice also declined significantly. Compared with model group, the PNS group had lower levels of body weight growth, food consumption, adipose tissue, and leptin (P < 0.05). Lower FBG level was also found in Rb1 treated mice (12 d of administration), P < 0.05.. PNS has anti-hyperglycemic and anti-obesity activities by improving insulin and leptin sensitivities in KK-Ay mice. Rb1 may be the hypoglycemic ingredient in the PNS extract.

    Topics: Adipose Tissue; Animals; Body Weight; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Drugs, Chinese Herbal; Ginsenosides; Hypoglycemic Agents; Insulin; Insulin Resistance; Leptin; Lipids; Mice; Mice, Inbred C57BL; Obesity; Panax notoginseng; Saponins

2014
Ginsenoside Rd attenuates the inflammatory response via modulating p38 and JNK signaling pathways in rats with TNBS-induced relapsing colitis.
    International immunopharmacology, 2012, Volume: 12, Issue:2

    In this study, we investigated the effects and the protective mechanism of ginsenoside Rd (GRd) which has been identified as one of the effective compounds from ginseng on relapsing colitis model induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS) in rats. After inducing relapsing colitis in experimental rats on two occasions by intracolonic injection of TNBS, GRd (10, 20 and 40 mg/kg) was administered to experimental colitis rats for 7 days. The inflammatory degree was assessed by macroscopic score, histology and myeloperoxidase (MPO) activity. The levels of proinflammatory cytokines, such as TNF-α, IL-1β, and IL-6 were determined by ELISA. Mitogen-activated protein kinase (MAPK) phosphorylation was analyzed by western blotting method. The results showed that GRd markedly attenuates the inflammatory response to TNBS-induced relapsing colitis, as evidenced by improved signs, increased body weight, decreased colonic weight/length ratio, reduced colonic macroscopic and microscopic damage scores, inhibited the activity of MPO, lowered proinflammatory cytokine levels and suppressed phosphorylation of p38 and JNK. The possible mechanism of protection on experimental colitis after GRd administration was that it could reduce the accumulation of leukocytes and down-regulate multiple proinflammatory cytokines through modulation of JNK and p38 activation.

    Topics: Animals; Body Weight; Colitis; Colon; Down-Regulation; Ginsenosides; Interleukin-1beta; Interleukin-6; Leukocytes; Male; MAP Kinase Kinase 4; MAP Kinase Signaling System; Mitogen-Activated Protein Kinases; p38 Mitogen-Activated Protein Kinases; Peroxidase; Phosphorylation; Rats; Rats, Wistar; Trinitrobenzenesulfonic Acid; Tumor Necrosis Factor-alpha

2012