Enhanced Anti-Inflammatory Effects of Silibinin and Capsaicin Combination in Lipopolysaccharide-Induced RAW264.7 Cells by Inhibiting NF-κB and MAPK Activation

Zheng, Yingying; Chen, Jie; Wu, Xiao-Zheng; Zhang, Xin; Hu, Chunmei; Kang, Yu; Lin, Jing; Li, Jiamin; Huang, Yuechang; Zhang, Xingmin; Li, Chen

doi:10.3389/fchem.2022.934541

Cited by 6 publications

(3 citation statements)

References 31 publications

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“…Importantly, the combination of SB and thymol (40 µM and 120 µM, respectively) demonstrated a more pronounced protective effect in comparison to the single usage of SB [42]. On the same line, the increased anti-inflammatory actions of SB and capsaicin combination in LPS-induced RAW264.7 cells was due to the suppression of NF-κB and MAPK activation [43]. The in vitro results obtained with RAW264.7 cells showed that SB suppressed RANKL-induced nuclear factor of activated T cells 1 (NFATc1) induction and translocation via the NF-κB and MAPK signalling pathways.…”

Section: Macrophagesmentioning

confidence: 90%

Silymarin and Inflammation: Food for Thoughts

Surai,

Earle-Payne

2024

Antioxidants

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Inflammation is a vital defense mechanism, creating hostile conditions for pathogens, preventing the spread of tissue infection and repairing damaged tissues in humans and animals. However, when inflammation resolution is delayed or compromised as a result of its misregulation, the process proceeds from the acute phase to chronic inflammation, leading to the development of various chronic illnesses. It is proven that redox balance disturbances and oxidative stress are among major factors inducing NF-κB and leading to over-inflammation. Therefore, the anti-inflammatory properties of various natural antioxidants have been widely tested in various in vitro and in vivo systems. Accumulating evidence indicates that silymarin (SM) and its main constituent silibinin/silybin (SB) have great potential as an anti-inflammation agent. The main anti-inflammatory mechanism of SM/SB action is attributed to the inhibition of TLR4/NF-κB-mediated signaling pathways and the downregulated expression of pro-inflammatory mediators, including TNF-α, IL-1β, IL-6, IL-12, IL-23, CCL4, CXCL10, etc. Of note, in the same model systems, SM/SB was able to upregulate anti-inflammatory cytokines (IL-4, IL-10, IL-13, TGF-β, etc.) and lipid mediators involved in the resolution of inflammation. The inflammatory properties of SM/SB were clearly demonstrated in model systems based on immune (macrophages and monocytes) and non-immune (epithelial, skin, bone, connective tissue and cancer) cells. At the same time, the anti-inflammatory action of SM/SB was confirmed in a number of in vivo models, including toxicity models, nonalcoholic fatty liver disease, ischemia/reperfusion models, stress-induced injuries, ageing and exercising models, wound healing and many other relevant model systems. It seems likely that the anti-inflammatory activities of SM/SB are key elements on the health-promoting properties of these phytochemicals.

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Section: Macrophagesmentioning

confidence: 90%

Silymarin and Inflammation: Food for Thoughts

Surai,

Earle-Payne

2024

Antioxidants

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“…The vanillyl moiety of capsaicin is majorly responsible for its bioactivity and is used widely for the treatment of chronic musculoskeletal and neuropathic pain, chronic migraines and in treating functional dyspepsia ( 186 , 187 ). Capsaicin also shows an anti-inflammatory effect by down-regulating LPS-induced expression of COX-2 and NF-κB in RAW 264.7 macrophages ( 188 ). Capsaicin has similarly been found to suppress the LPS-induced expression of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 in THP-1 macrophages ( 189 ).…”

Section: Bioactives and Osteoarthritis: Metabolic And Anti-inflammato...mentioning

confidence: 99%

Bioactives and their roles in bone metabolism of osteoarthritis: evidence and mechanisms on gut-bone axis

Basak,

Hridayanka,

Duttaroy

2024

Front. Immunol.

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Bioactives significantly modify and maintain human health. Available data suggest that Bioactives might play a beneficial role in chronic inflammatory diseases. Although promised, defining their mechanisms and opting to weigh their benefits and limitations is imperative. Detailed mechanisms by which critical Bioactives, including probiotics and prebiotics such as dietary lipids (DHA, EPA, alpha LA), vitamin D, polysaccharides (fructooligosaccharide), polyphenols (curcumin, resveratrol, and capsaicin) potentially modulate inflammation and bone metabolism is limited. Certain dietary bioactive significantly impact the gut microbiota, immune system, and pain response via the gut-immune-bone axis. This narrative review highlights a recent update on mechanistic evidence that bioactive is demonstrated demonstrated to reduce osteoarthritis pathophysiology.

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“…11 In addition, CAP has also exerted significant therapeutic effects on acute liver injury, 12 colitis, 13 and LPS-induced inflammation in macrophages. 14 Currently, there are various ointments containing CAP that can be topically applied to alleviate pain, migraines, headaches, psoriasis, and infections caused by the herpes simplex virus. 15,16 Additionally, CAP has shown promising therapeutic potential in mitigating symptoms related to dyspepsia, decreased appetite, excessive gas, arterial plaque buildup, cardiovascular disorders, and muscle tension.…”

Section: Introductionmentioning

confidence: 99%

Capsaicin Attenuates LPS-Induced Acute Lung Injury by Inhibiting Inflammation and Autophagy Through Regulation of the TRPV1/AKT Pathway

Hu,

Liu,

Wang

et al. 2024

JIR

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Acute lung injury (ALI) is a severe pulmonary disease characterized by damage to the alveoli and pulmonary blood vessels, leading to severe impairment of lung function. Studies on the effect of capsaicin (8-methyl-N-geranyl-6-nonamide, CAP) on lipopolysaccharide (LPS)-induced ALI in bronchial epithelial cells transformed with Ad12-SV40 2B (BEAS-2B) are still limited. This study aimed to investigate the effect and specific mechanism by which CAP improves LPS-induced ALI. Methods: The present study investigated the effect of CAP and the potential underlying mechanisms in LPS-induced ALI in vitro and vivo via RNA sequencing, Western blotting (WB), quantitative real-time reverse transcription PCR (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), and transmission electron microscopy (TEM). The TRPV1 inhibitor AMG9810 and the AKT agonist SC79 were used to confirm the protective effect of the TRPV1/AKT axis against ALI. The autophagy agonist rapamycin (Rapa) and the autophagy inhibitors 3-methyladenine (3-MA) and bafilomycin A1 (Baf-A1) were used to clarify the characteristics of LPSinduced autophagy. Results: Our findings demonstrated that CAP effectively suppressed inflammation and autophagy in LPS-induced ALI, both in vivo and in vitro. This mechanism involves regulation by the TRPV1/AKT signaling pathway. By activating TRPV1, CAP reduces the expression of P-AKT, thereby exerting its anti-inflammatory and inhibitory effects on pro-death autophagy. Furthermore, prior administration of CAP provided substantial protection to mice against ALI induced by LPS, reduced the lung wet/dry ratio, decreased proinflammatory cytokine expression, and downregulated LC3 expression. Conclusion: Taken together, our results indicate that CAP protects against LPS-induced ALI by inhibiting inflammatory responses and autophagic death through the TRPV1/AKT signaling pathway, presenting a novel strategy for ALI therapy.

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Enhanced Anti-Inflammatory Effects of Silibinin and Capsaicin Combination in Lipopolysaccharide-Induced RAW264.7 Cells by Inhibiting NF-κB and MAPK Activation

Cited by 6 publications

References 31 publications

Silymarin and Inflammation: Food for Thoughts

Silymarin and Inflammation: Food for Thoughts

Bioactives and their roles in bone metabolism of osteoarthritis: evidence and mechanisms on gut-bone axis

Capsaicin Attenuates LPS-Induced Acute Lung Injury by Inhibiting Inflammation and Autophagy Through Regulation of the TRPV1/AKT Pathway

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