Work is currently planned to assess the nature of nimbolide protect against doxorubicin (DOX) -treated myocardial damage. myocardial damage produced by 2.5 mg / kg DOX was given on alternate days (14 days). Thiobarbituric reactive substances of acid (TBARS) levels of lipid markers of peroxidative lifted, while reducing weight, the weight of the heart, the index of blood pressure and reduce blood levels of antioxidants such as glutathione-S-transferase, superoxide dismutase, catalase, glutathione peroxidase, glutathione and glutathione reductase observed in heart tissue of DOX-treated animals.

DOX-treated animals showed levels plus cardiac markers like monocytes chemotactic protein -1, interferon-gamma, aspartate transferase, creatine kinase, lactate dehydrogenase, creatine kinase-muscle / brain, heart-type fatty acid binding protein , glycogen phosphorylase isoenzyme BB, transforming growth factor-β, brain natriuretic peptide, myoglobin, and cTnI in serum. Histopathological assessment confirms DOX-induced cardiotoxicity.

rat Furthermore, DOX-induced showed augmented inflammatory mediators (factor-kB nuclear [NF-kB], tumor necrosis factor-α [TNF-α], and interleukin-1β [IL-1β]) and increased PI 3 < / em> K / Akt signaling protein (PI 3 K, p-Bad / Bad, caspase- 3 , and p-Akt), while decreasing oxidative markers (HO-1 and NQO-1) and p-PTEN was observed. Nimbolide mice supplements showed decreased activity / cardiac marker levels and TBARS levels in serum and liver tissue.

Enzymatic antioxidant levels and nonenzimatik plus the supplement nimbolide rat heart tissue. Nimbolide effect of a decrease in apoptosis, inflammation, and enhance antioxidant markers through modulation of p-Bad / Bad, caspase- 3 , PI 3 K, p-Akt, TNF-α, NF -kB, IL-1β, HO-1, NQO-1 and p-PTEN markers. Explanation histopathology was observed in line with biochemical analysis. Therefore, the findings of the current work is that nimbolide has defensive effect on the myocardium of the heart tissue damage DOX-induced.

Nimbolide prevents myocardial damage by regulating cardiac biomarkers, antioxidant level, and apoptosis signaling against doxorubicin-induced cardiotoxicity in rats
Nimbolide prevents myocardial damage by regulating cardiac biomarkers, antioxidant level, and apoptosis signaling against doxorubicin-induced cardiotoxicity in rats

Monocyte chemotactic protein-1 plays a role in ovarian dysfunction associated with high-fat diet-induced obesity

Obesity, known to cause systemic elevation in monocytes chemotactic protein -1 (MCP-1), adversely affecting normal ovarian function. The purpose of this study was to determine whether MCP-1 plays a role in ovarian dysfunction associated with obesity caused by a high fat (HF) diet intake. The wild-type (WT) C57BL / 6J mice were fed either a normal chow (NC) (Group 1, control group) or HF diet (Group 2). To assess whether MCP-1 is involved in ovarian dysfunction HF-diet-induced, MCP-1 knockout mice fed the HF diet (Group 3 ).

weight, body fat composition, the number of oocytes collected following ovarian superovulation with gonadotropins, ovarian macrophage markers and expression of genes important in folliculogenesis and steroidogenesis measured in the 3 group of animals. Animals in Group 2 gained significant weight and body mass, resulting in the fewest number of oocytes following superovulation, and has a significant change in the genes involved in ovarian folliculogenesis and steroidogenesis as well as genes involved in inflammation.

While the animals in Group 3 weight and body fat composition is highest, they produce the same number of oocytes compared to animals in Group 1, but has a different ovarian gene expression compared to Group 2. These findings indicate that MCP -1 gene knockout can reverse some of the adverse effects of obesity caused by the intake of the HF diet.


B6266-10 10 mg
EUR 211.2


B6266-25 25 mg
EUR 420


B6266-5 5 mg
EUR 139.2


HY-100371 100mg
EUR 1135.2


HY-100406 5mg
EUR 159.6

(RS)-MCPG disodium salt

B7476-10 10 mg
EUR 362.4

(RS)-MCPG disodium salt

B7476-50 50 mg
EUR 1336.8

Future studies assessing ovarian histology in MCP-1 immobilize a mouse model will confirm our findings. MCP-1 inhibition may represent a future therapeutic target to protect the health of the ovaries from the adverse effects of HF diet consumption.