Inflammation plays an important role in host defense against external stimuli such as infection by pathogen, endotoxin or chemical exposure by the production of the inflammatory mediators that produced by macrophage. Anti-inflammatory factor is important to treat the dangers of chronic inflammation associated with chronic disease. This research aims to analyze the anti-inflammatory effects of Garcinia mangostana L. peel extract (GMPE), α-mangostin, and γ-mangostin in LPS-induced murine macrophage cell line (RAW 264.7) by inhibiting the production of inflammatory mediators. The cytotoxic assay of G. mangostana L. extract, α-mangostin, and γ-mangostin were performed by MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) to determine the safe and non-toxic concentration in RAW 264.7 for the further assay. The concentration of inflammatory mediators (COX-2, IL-6, and IL-1β) were measured by the ELISA-based assay and NO by the nitrate/nitrite colorimetric assay in treated LPS-induced RAW 264.7 cells. The inhibitory activity was determined by the reducing concentration of inflammatory mediators in treated LPS-induced RAW 264.7 over the untreated cells. This research revealed that GMPE, α-mangostin, and γ-mangostin possess the anti-inflammatory effect by reducing COX-2, IL-6, IL-1β, and NO production in LPS-induces RAW 264.7 cells.
Cell Line ; Chronic Disease ; Fibrinogen ; Garcinia mangostana* ; Inflammation ; Interleukin-6 ; Macrophages ; RAW 264.7 Cells

Dyslipidemia is a condition of fat metabolism disorders with increased levels of total cholesterol (CHOL), triglycerides (TG), low-density lipoprotein (LDL), and low high-density lipoprotein (HDL). Dyslipidemia is often found in patients with type 2 diabetes mellitus (DMT2) with a higher risk of cardiovascular disease.The extract of butterfly pea (Clitoria ternatea L.) (CTE), exhibits therapeutic action like antioxidant, antiinflammatory and antidiabetic properties. This study examined the antidiabetic potential of CTE in rat models of dyslipidemia and DM. Rats were fed nicotinamide (NA) and streptozotocin (STZ) to induce DMT2 after a 28-day high-fat diet, and the rats were given with CTE at 200, 400, 800 mg/kg body weight (BW), glibenclamide, and simvastatin for 28 days. Suppressor of mothers against decapentaplegic homolog 3 (SMAD3), and SMAD4 were assayed by immunohistochemistry (IHC), regenerating family member 1 alfa (REG1A), REG1B and glucagon gene expression were measured by quantitative reverse transcription polymerase chain reaction (RTqPCR) body weight was measured weekly. CTE at a dose of 800 mg/kg BW was the most active to increase body weight, and decrease SMAD3, SMAD4 protein expression, glucagon, REG1A, REG1B genes expression in dyslipidemia and DM rat model. CTE has potency antidiabetic activities in dyslipidemia and DM rat mode