scholarly journals Dietary Rice Bran Oil and γ‐Oryzanol Attenuates Toll Like Receptor‐mediated IκBα Phosphorylation, NF‐κB p65 Activation and Matrix Metallo Protease‐9 Expression in Peritoneal Macrophages from Rats Fed Partially Hydrogenated Vegetable Fat and thereby Exhibit Anti‐Inflammatory Activity

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Poorna C Yalagala ◽  
Sugasini Dhavamani ◽  
Pavan Kumar Pandugala ◽  
B.R. Lokesh
2022 ◽  
Vol 10 (B) ◽  
pp. 1-12
Author(s):  
Lilis Lisnawati ◽  
Sri Poeranto ◽  
Agustina Tri Endharti ◽  
Moch. Istiadjid Edi Santoso

BACKGROUND: Fertility is affected by both the reproductive organs and external factors (genetics, hormones, radiation exposure, use of insecticides, and nutrition). The histological structure of the ovaries is an indicator of reproductive function. Insect repellent use with pyrethroid active ingredients and its impact on health has become a discussion in the medical sector for years. Disruption of the reproductive system homeostasis may cause several issues, from disruption of ovarian function to infertility. γ-Oryzanol has higher antioxidants than vitamin E. It is found mostly in rice bran oil (RBO). Researchers have investigated the effectiveness of RBO and γ-Oryzanol, but the number of studies focusing on the reproductive system is very limited. Results of in silico showed anti-inflammatory potential, and nitric oxide γ-Oryzanol is stronger than the antioxidant activity. It also showed γ-Oryzanol bond with Foxo3a and Growth Differentiating Factor 9 (GDF9), indicating the γ-Oryzanol potential for reproductive health (women). Studies also reported that γ-Oryzanol administration caused anti-inflammatory and antioxidant activity compared to RBO in improving ovarian physiological function using tumor necrosis factor α (TNF-α) levels, Foxo3a expression, and GDF9 expression exposed to one push transfluthrin as the parameter. AIM: We aimed to investigate antioxidant and anti-inflammatory activity of γ-Oryzanol compared to rice bran oil to repair ovarian histological structure from one push transfluthrin exposure effect. METHODS: Experimental research, post-test only control group design approach, with a completely randomized design, consisted of 6 (six) groups of Wistar strain female rats. They were exposed to one push with the active ingredient of transfluthrin 21.3%, by inhalation for 6 hours, RBO 0.3 mg/g/ body weight (BW)/day, γ-Oryzanol 3.75 ml/g/BW/day. Statistical analysis was done with the Mann Whitney’s posthoc Kruskal Wallis test with IBM SPSS version 25 software. RESULTS: γ-Oryzanol had more potent anti-inflammatory and antioxidant activity than RBO in improving the ovarian histology structure (including maintaining ovarian weight, increasing follicular growth, and suppressing follicular abnormalities) through decreased TNF-α levels and decreased Foxo3a expression, and increased GDF9 expression. CONCLUSION: The administration of γ-Oryzanol improves the ovarian histological structure from free radicals effects, namely exposure to one push of transfluthrin.


2018 ◽  
Vol 40 (1) ◽  
pp. 51-55
Author(s):  
Pavithra K. Balasubramanian ◽  
Jieun Kim ◽  
Kkabi Son ◽  
Prasannavenkatesh Durai ◽  
Yangmee Kim

2015 ◽  
Vol 10 (12) ◽  
pp. 2697-2705 ◽  
Author(s):  
Vincent Flacher ◽  
Patrick Neuberg ◽  
Floriane Point ◽  
François Daubeuf ◽  
Quentin Muller ◽  
...  

Author(s):  
Jaeyong Kim ◽  
Gyuok Lee ◽  
Huwon Kang ◽  
Ji-Seok Yoo ◽  
Yongnam Lee ◽  
...  

Background: Inflammation is emerging as a key contributor to many vascular diseases and furthermore plays a major role in autoimmune diseases, arthritis, allergic reactions, and cancer. Lipopolysaccharide (LPS), which is a component constituting the outer membrane of Gram-negative bacteria, is commonly used for an inflammatory stimuli to mimic inflammatory diseases. Nuclear factor-kappa B (NF-κB) is a transcription factor and regulates gene expression particularly related to the inflammatory process. Stauntonia hexaphylla (Lardizabalaceae) is widely used as a traditional herbal medicine for rheumatism and osteoporosis and as an analgesic, sedative, and diuretic in Korea, Japan, and China. Objective: The purpose of this study was to investigate the anti-inflammatory activity of YRA-1909, the leaf aqueous extract of Stauntonia hexaphylla using LPS-activated rat peritoneal macrophages and rodent inflammation models. Results: YRA-1909 inhibited the LPS-induced nitric oxide (NO) and proinflammatory cytokine production in rat peritoneal macrophages without causing cytotoxicity and reduced inducible NO synthase and prostaglandin E2 levels without affecting the cyclooxygenase-2 expression. YRA-1909 also prevented the LPS-stimulated Akt and NF-κB phosphorylation and reduced the carrageenan-induced hind paw edema, xylene-induced ear edema, acetic acid-induced vascular permeation, and cotton pellet-induced granuloma formation in a dose-dependent manner in mice and rats. Conclusions: S. hexaphylla leaf extract YRA-1909 had anti-inflammatory activity in vitro and in vivo that involves modulation of Akt/NF-κB signaling. Thus, YRA-1909 is safe and effective for the treatment of inflammation.


2021 ◽  
Vol 8 (10) ◽  
Author(s):  
Chen G ◽  
◽  
Liu Y ◽  
Zhang M ◽  
Xu Y ◽  
...  

Niloticin is an active compound from Cortex phellodendri, but its antiinflammatory activity has not yet been explored. The aim of the present study was to assess the drug potential of niloticin and to study the MD-2-targeting mechanism of its anti-inflammatory activity. Niloticin’s drug potential was analyzed using the Traditional Chinese Medicine Systems Pharmacology Database. Molecular docking and biolayer interferometry technology were used to explore the anti-inflammatory mechanism of niloticin by targeting myeloid differentiation protein 2 (MD-2), which mediates a series of Toll-Like Receptor (TLR) 4-dependent inflammatory responses. The cytokines involved in the LPSTLR4/ MD-2-NF-κB pathway were evaluated by ELISA, RT-PCR, and western blot. The results showed that niloticin has drug potential and could bind to MD- 2. Niloticin had no impact on cell viability. Niloticin could significantly decrease the levels of NO, IL-6, TNF-a, and IL-1β (P<0.01) induced by LPS. IL-1β, IL-6, iNOS, TNF-a, and COX-2 mRNA expression levels were decreased by niloticin (all P<0.01). Compared with the control group, TLR4, p65, MyD88, p-p65, and iNOS expression levels induced by LPS were suppressed by niloticin (all P<0.01). In conclusion, niloticin is a potential MD-2 antagonist. It might interact with MD-2 to play an anti-inflammatory role by suppressing the activation of the LPS-TLR4/MD-2-NF-κB signaling pathway.


2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Shi Hyoung Kim ◽  
Jae Gwang Park ◽  
Jongsung Lee ◽  
Woo Seok Yang ◽  
Gye Won Park ◽  
...  

Even though a lot of reports have suggested the anti-inflammatory activity of kaempferol (KF) in macrophages, little is known about its exact anti-inflammatory mode of action and its immunopharmacological target molecules. In this study, we explored anti-inflammatory activity of KF in LPS-treated macrophages. In particular, molecular targets for KF action were identified by using biochemical and molecular biological analyses. KF suppressed the release of nitric oxide (NO) and prostaglandin E2(PGE2), downregulated the cellular adhesion of U937 cells to fibronectin (FN), neutralized the generation of radicals, and diminished mRNA expression levels of inflammatory genes encoding inducible NO synthase (iNOS), TNF-α, and cyclooxygenase- (COX-) 2 in lipopolysaccharide- (LPS-) and sodium nitroprusside- (SNP-) treated RAW264.7 cells and peritoneal macrophages. KF reduced NF-κB (p65 and p50) and AP-1 (c-Jun and c-Fos) levels in the nucleus and their transcriptional activity. Interestingly, it was found that Src, Syk, IRAK1, and IRAK4 responsible for NF-κB and AP-1 activation were identified as the direct molecular targets of KF by kinase enzyme assays and by measuring their phosphorylation patterns. KF was revealed to havein vitroandin vivoanti-inflammatory activity by the direct suppression of Src, Syk, IRAK1, and IRAK4, involved in the activation of NF-κB and AP-1.


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