Abstract
Gymnema inodorum (Lour.) Decne. (G. inodorum) is widely used in Northern Thai cuisine as local vegetables and commercial herb tea products. In the present study, G. inodorum extract (GIE) was evaluated for its antioxidant and anti-inflammatory effects in LPS plus IFN-γ-induced RAW264.7 cells. Major compounds in GIE were evaluated using GC-MS and found 16 volatile compounds presenting in the extract. GIE exhibited antioxidant activity by scavenging the intracellular reactive oxygen species (ROS) production and increasing superoxide dismutase 2 (SOD2) mRNA expression in LPS plus IFN-γ-induced RAW264.7 cells. GIE showed anti-inflammatory activity through suppressing nitric oxide (NO), proinflammatory cytokine production interleukin 6 (IL-6) and also downregulation of the expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and IL-6 mRNA levels in LPS plus IFN-γ-induced RAW264.7 cells. Mechanism studies showed that GIE suppressed the NF-κB p65 nuclear translocation and slightly decreased the phosphorylation of NF-κB p65 (p-NF-κB p65) protein. Our studies applied the synchrotron radiation-based FTIR microspectroscopy (SR-FTIR), supported by multivariate analysis, to identify the FTIR spectral changes based on macromolecule alterations occurring in RAW264.7 cells. SR-FTIR results demonstrated that the presence of LPS plus IFN-γ in RAW264.7 cells associated with the increase of amide I/amide II ratio (contributing to the alteration of secondary protein structure) and lipid content, whereas glycogen and other carbohydrate content were decreased. These findings lead us to believe that GIE may prevent oxidative damage by scavenging intracellular ROS production and activating the antioxidant gene, SOD2, expression. Therefore, it is possible that the antioxidant properties of GIE could modulate the inflammation process by regulating the ROS levels, which lead to the suppression of proinflammatory cytokines and genes. Therefore, GIE could be developed into a novel antioxidant and anti-inflammatory agent to treat and prevent diseases related to oxidative stress and inflammation.
Highlights
Inflammation is the immune system’s response to harmful stimuli, such as infection and tissue injury [1]
The present study indicates that the suppressive effect of G. inodorum extract (GIE) on nitric oxide (NO) production is mediated through the inhibition of inducible nitric oxide synthase (iNOS) mRNA expression
The results indicated that GIE at all testedconcentration significantly suppressed LPS plus IFN-γinduced interleukin 6 (IL-6) production (p < 0:05; Figure 2(a)) and slightly decreased TNF-α production compared to untreated LPS plus IFN-γ-induced cells (IN) (Figure 2(b))
Summary
Inflammation is the immune system’s response to harmful stimuli, such as infection and tissue injury [1]. Due to the response with the existence of cellular stimuli, activated macrophages produce high levels of proinflammatory cytokines, including IL-6, interleukin 1β (IL-1β), TNF-α, and prostaglandin (PGE2) [6]. These cytokines are involved in the process of pathological pain. The link between oxidative stress and inflammation has extensively been demonstrated that the mechanism by which continued oxidative stress can lead to chronic inflammation This mechanism leads to various inflammatory diseases such as diabetes, cardiovascular diseases, cancer, degenerative diseases, ischemia, and anemia [8]. The necessity for exploring a better anti-inflammatory therapeutic agent is always in need
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