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Cassia alata, a traditional herb with a global presence, is renowned for its anti-inflammatory, antibacterial, and antifungal properties, making it a go-to remedy for skin ailments. While it has demonstrated wound healing capabilities in both in vitro and in vivo studies, the precise mechanisms remain elusive. This review aims to highlight its key phytochemicals, their effects, and the mechanism of action. The compounds that have been reviewed and discussed include kaempferol, apigenin, quercetin, rhein, and rutin. These polyphenols play important roles in normal and impaired wound healing processes, encompassing hemostasis, inflammation, proliferation, and tissue remodeling. [ABSTRACT FROM AUTHOR]

The stimulator of interferon genes (STING) signaling pathway is crucial for the pathogenesis of autoimmune and inflammatory disorders, including acute lung injury (ALI). Apigenin (4 ′ ,5,7-trihydroxyflavone) is a natural flavonoid widely found in fruits, vegetables, and Chinese medicinal herbs that exhibits a range of pharmacological effects, such as antibacterial and anti-inflammatory activities. However, the efficacy of apigenin in STING pathway-mediated diseases remains unclear. Accordingly, this study screened Chinese medicines to identify potent agents that reduced the synthesis of type I interferons (IFNs). The results revealed apigenin as a potent compound with low cytotoxicity that markedly reduced the synthesis of type I IFNs in response to STING pathway agonists. Besides, apigenin markedly suppressed innate immune responses triggered by the STING agonist SR-717. Mechanistically, apigenin downregulated IFN beta 1 (IFNB1) expression mediated by the STING pathway via dose-dependent inhibition of STING expression, reduction of dimerization, nuclear translocation of phosphorylated IRF3, and disruption of the association between STING and IRF3. Moreover, apigenin effectively mitigated pathological pulmonary inflammation and lung edema in lipopolysaccharide (LPS)-induced ALI in mice. Apigenin further strongly attenuated the hallmarks of immoderate inflammation (interleukin (IL)-6, IL-1 β , and tumor necrosis factor α) and innate immune responses (IFNB1, C-X-C motif chemokine ligand 10, and IFN-stimulated gene 15) by preventing the activation of the STING/IRF3 pathway both in vitro and in vivo. Importantly, SR-717 significantly reversed the inhibitory effects of apigenin in LPS-induced THP1-BlueTM ISG macrophages. Collectively, apigenin effectively alleviated innate immune responses and mitigated inflammation in LPS-induced ALI via inhibition of the STING/IRF3 pathway. These findings suggest the potential of apigenin as a prophylactic and therapeutic candidate for managing STING-mediated diseases. [ABSTRACT FROM AUTHOR]

Background: Apigenin has been reported to exhibit anti-inflammatory and anti-oxidative activities. This study aimed to investigate the protective role of Apigenin on chemotherapy-induced peripheral neuropathy (CIPN). Methods: CIPN mouse model was established using Paclitaxel treatment. Hot plate and tail prick latency tests were performed to examine the allodynia and hyperalgesia behaviors. Antiinflammatory and anti-oxidative effects of Apigenin on CIPN were determined by enzyme-linked immunosorbent (ELISA) assay, Western blot, and qRT-PCR. Nuclear recruitment of nuclear factor erythroid 2-related factor 2 (NRF2) was analyzed to evaluate the underlying mechanisms of the protective effects of Apigenin. Results: Apigenin significantly alleviated CIPN-induced nociceptive behaviors of CIPN mice. It also decreased the TNF-α and IL-1β levels, suppressed oxidative stress and inflammation in the surgical spinal cord tissues. Mechanistically, Apigenin altered the pro-inflammatory and anti-inflammatory phenotypes ratio of microglia through promoting the nuclear recruitment of NRF2 and activating the NRF2/Antioxidant Response Element (ARE) signaling pathway. Conclusions: In summary, Apigenin relieves CIPN by regulating microglia activation and polarization, which provides a potential therapeutic strategy for CIPN treatment. [ABSTRACT FROM AUTHOR]

Apigenin is a plant flavone proven with biological properties such as anti-inflammatory, antioxidant, and antimicrobial effects. This study, it was aimed to examine the possible anti-inflammatory, antioxidant, and neuroprotective effects of apigenin in the setting of the mild traumatic brain injury (TBI) model. Wistar albino male rats were randomly assigned to groups: control (n = 9), TBI (n = 9), TBI + vehicle (n = 8), and TBI + apigenin (20 and 40 mg/kg, immediately after trauma; n = 6 and n = 7). TBI was performed by dropping a 300 g weight from a height of 1 m onto the skull under anesthesia. Neurological examination and tail suspension tests were applied before and 24 h after trauma, as well as Y-maze and object recognition tests, after that rats were decapitated. In brain tissue, luminol- and lucigenin-enhanced chemiluminescence levels and cytokine ELISA levels were measured. Histological damage was scored. Data were analyzed with one-way ANOVA. After TBI, luminol (p <.001) and lucigenin (p <.001) levels increased, and luminol and lucigenin levels decreased with apigenin treatments (p <.01–.001). The tail suspension test score increased with trauma (p <.01). According to the pre-traumatic values, the number of entrances to the arms (p <.01) in the Y-maze decreased after trauma (p <.01). In the object recognition test, discrimination (p <.05) and recognition indexes (p <.05) decreased with trauma. There was no significant difference among trauma apigenin groups in behavioral tests. Interleukin (IL)-10 levels, one of the anti-inflammatory cytokines, decreased with trauma (p <.05), and increased with 20 and 40 mg apigenin treatment (p <.001 and p <.01, respectively). The histological damage score in the cortex was decreased in the apigenin 20 mg treatment group significantly (p <.05), but the decrease observed in the apigenin 40 mg group was not significant. The results of this study revealed that apigenin 20 and 40 mg treatment may have neuroprotective effects in mild TBI via decreasing the level of luminol and lucigenin and increasing the IL-10 levels. Additionally, apigenin 20 mg treatment ameliorated the trauma-induced cortical tissue damage. [ABSTRACT FROM AUTHOR]

Apigenin is one of the flavonoids found in abundance in various natural sources, including fruits and vegetables, with important functions in the prevention and treatment of various health problems. It is known that apigenin, which has a very high pharmacological activity, has mainly antioxidant, anti-inflammatory and anti-neoplastic effects, and exhibits these effects by up-or down-regulating proteins in specific pathways. This study focused on the effects of apigenin on inflammation, oxidant-antioxidant balance, cancer, apoptosis and cell cycle, and these properties were supported by in vivo and in vitro studies. As a result of the researches, it was concluded that apigenin exhibits anti-inflammatory, antioxidant and anti-carcinogenic properties. Moreover, it has been observed that apigenin leads damaged, worn or cancerous cells to apoptosis, inhibits the proliferation of such cells by stopping the cell cycle at various checkpoints, and thus exhibits an antiproliferative effect. [ABSTRACT FROM AUTHOR]

Apigenin (4,'5,7-trihydroxyflavone) is one of the most studied flavonoids with low toxicity and abundantly present phenolic compound in the plant kingdom. The main sources of apigenin are fruits, vegetables, nuts, herbs, honey, and plant-based drinks like tea. Numerous plants produce apigenin as a secondary metabolite and its intake is strongly related to its anti-inflammatory propensities. The purpose of present review was to wade through the literature on the anti-inflammatory mechanisms of this metabolite in various diseases and summarize the key objectives as they appear. Existing literature reported that apigenin is a promising candidate in managing a panoply of inflammatory-related diseases including cancer, diabetes, obesity, depression, insomnia, infection, and respiratory, cardiovascular, hepatoprotective, neurodegenerative, and skin diseases. Studies showed that apigenin significantly decreases the secretion of various proinflammatory cytokines specifically tumor necrosis factor (TNF)-α, IL-1β, IL-6, and IL-10. Moreover, apigenin effectively blocks the nitric oxide-mediated cyclooxygenase-2 expression and monocyte attachment and Prostaglandin by lowering iNOS and COX-2 in both microglial and macrophage mouse cells. Apigenin can slow the course of nonalcoholic fatty liver disease (NAFLD) in vivo by reducing high fat diet (HFD)-induced deposition of lipids and oxidative stress. It also controlled redox imbalances, suppress neuronal death and showed memory enhancement/learning skills and a reduction of fibrillar amyloid deposits with lowered insoluble Aβ concentrations in vivo. Taken together, it can be argued that apigenin can wane inflammation and thus offers a promising future in slowing down the development of chronic diseases and associated complications. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is a progressive hypokinetic movement disorder caused by selective degeneration of dopaminergic neurons in striatum and dopamine deficiency in a region of the midbrain. LPS is an endotoxin, used as animal model to induce microglial activation, neuroinflammation, oxidative stress, and neurotransmitter alteration with PD-like symptoms. Therefore, to prevent neuroinflammation and neurotransmitter changes and to restore normal brain physiology, we tried apigenin (AGN) alone and in combination with piperine (bioenhancer), in LPS experimental model of rats. In this study, rats were treated with single unilateral intranigral injection of LPS at a dose of 5 μg/5 μl on day 0. The oral administration of AGN (25 and 50 mg/kg; p.o.) alone, AGN (25 mg/kg; p.o.) in combination with piperine (2.5 mg/kg; p.o.), and bromocriptine (10mg/kg; p.o.) started from day 7th once in a day. Intranigral injection of LPS significantly altered body weight and behavioral parameters assessed on weekly basis. Furthermore, the biochemical and neuroinflammatory analysis confirmed (on day 22nd) increased level of nitrite, MDA, SOD, TNF-α, IL-1β, IL-6, and caspase-1, and decreased level of CAT, GSH, and complex-I. Furthermore, altered level of neurotransmitters (DA, GABA, and glutamate) and cellular changes were observed from histopathological and immunohistochemistry (NF-kB and Nrf-2) analysis. Treatment with AGN (25 and 50 mg/kg; p.o.) alone and AGN (25 mg/kg; p.o.) in combination with piperine (2.5 mg/kg; p.o.) significantly attenuated the alteration in body weight, motor impairments, oxidative stress, neuroinflammation, and neurotransmitters in rat brain. The neuroprotective effect of AGN against LPS-induced cell death is attributed by modulating NF-kB and Nrf2 signaling pathway in the striatum. [ABSTRACT FROM AUTHOR]

Background/objective: Apigenin is a member of the flavonoid family that can regulate various biological processes, which is characterized as a treatment of different inflammatory disorders and pathological problems associated with oxidative stress (OS). Recent research has focused on apigenin immunomodulatory properties as a potential treatment for different types of lung injuries. This meta-analysis was designed to determine the impact of apigenin treatment on inflammatory markers and OS parameters in animal models of lung injuries. Methods: The comprehensive literature search was conducted using electronic databases such as Google Scholar, PubMed, Web of Science, Scopus, and Embase up to August 2021. To assess apigenin's effect on inflammatory mediators and OS biomarkers in lung injury animal models, we used the I2 statistic to determine the heterogeneity. We then pooled data as standardized mean difference (SMD) with a 95% confidence interval (CI). Results: Our meta-analysis of the pooled data for inflammatory biomarkers demonstrated that the apigenin administration significantly decreased the NF-κB expression (SMD − 1.60, 95% CI [− 2.93 to − 0.26]; I2 = 89.0%, p < 0.001), IL-1β (SMD − 4.30, 95% CI [− 6.24 to − 2.37]; I2 = 67.3%, p = 0.047), IL-6 (SMD − 4.10, 95% CI [− 5.04 to − 3.16]; I2 = 72.6%, p < 0.001), TNF-α (SMD − 3.74, 95% CI [− 4.67 to − 2.82]; I2 = 84.1%, p < 0.001), and TNF-α gene expression (SMD − 3.44, 95% CI [− 4.44 to − 2.43]; I2 = 0.0%, p = 0.622). This study also indicated the efficacy of apigenin in increasing the level of CAT (SMD 4.56, 95% CI [3.57 to 5.55]; I2 = 15.3%, p = 3.15), GSH (SMD 5.12, 95% CI [3.53 to 6.70]; I2 = 77.6%, p < 0.001), and SOD (SMD 3.45, 95% CI [2.50 to 4.40]; I2 = 79.2%, p < 0.001), and decreasing the level of MDA (SMD − 3.87, 95% CI [− 5.25 to − 2.49]; I2 = 80.3%, p < 0.001) and MPO (SMD − 4.02, 95% CI [− 5.64 to − 2.40]; I2 = 88.9%, p < 0.001), TGF− β (SMD − 3.81, 95% CI [− 4.91 to − 2.70]; I2 = 73.4%, p = 0.001) and W/D level (SMD − 3.22, 95% CI [− 4.47 to − 1.97]; I2 = 82.1%, p < 0.001) than control groups. Conclusion: Overall, our findings showed the immunomodulatory potential of apigenin as an alternative treatment for the suppression of inflammatory responses and OS in different types of lung injury diseases. Nevertheless, due to the paucity of clinical studies, reliable preclinical models, and clinical settings, evaluating the influence of apigenin on lung injury is required in the future. Before conducting large-scale clinical trials, detailed human pharmacokinetic studies are also needed to establish dosage ranges and determine the initial safety and tolerability of apigenin. [ABSTRACT FROM AUTHOR]

• Apigenin might regulate the differentially altered protein (DEPs) while reducing inflammation in RA. • TNF-α activates the differential expression of pro-inflammatory cytokines, TTR, and RAGE via NF-kB pathway activation. • Anti-inflammatory effect of apigenin impedes TNF-α mediated dysregulation or expression associated with RA pathogenesis. Rheumatoid arthritis (RA) is a chronic inflammatory disease induced by TNF-α, which increases fibroblast-like synoviocytes inflammation, resulting in cartilage destruction. The current work sought to comprehend the pathophysiological importance of TNF-α stimulation on differential protein expression and their regulation by apigenin using in-vitro and in-vivo models of RA. The human RA synovial fibroblast cells were stimulated with or without TNF-α (10 ng/ml) and treated with 40 μM apigenin. In-silico, in-vitro and in-vivo studies were performed to confirm the pathophysiological significance of apigenin on pro-inflammatory cytokines and on differential expression of TTR and RAGE proteins. TNF-α induced inflammatory response in synoviocytes revealed higher levels of IL-6, IL-1β, and TNF-α cytokines and upregulated differential expression of TTR and RAGE. In-silico results demonstrated that apigenin has a binding affinity towards TNF-α, indicating its potential effect in the inflammatory process. Both in-vitro and in-vivo results obtained by Western Blot analysis suggested that apigenin reduced the level of p65 (p = 0.005), TTR (p = 0.002), and RAGE (p = 0.020). The findings of this study suggested that TNF-α promotes the differential expression of pro-inflammatory cytokines, TTR, and RAGE via NF-kB pathways activation. Anti-inflammatory effect of apigenin impedes TNF-α mediated dysregulation or expression associated with RA pathogenesis. [ABSTRACT FROM AUTHOR]

[Display omitted] • OL extracts presented anti-inflammatory, anti-cholinergic, and antioxidant activities. • Anti-cholinesterase activity of OL extracts was affected by flavonoids content. • COX-2 inhibitory activity was affected by secoiridoids. • Secoiridoid compounds and flavonoids equally affected to the antioxidant effects. In this study, the phytochemical profile of fifty olive leaves (OL) extracts from Spain, Italy, Greece, Portugal, and Morocco was characterized and their anti-cholinergic, anti-inflammatory, and antioxidant activities were evaluated. Luteolin-7 -O- glucoside, isoharmnentin, and apigenin were involved in the acetylcholinesterase (AChE) inhibitory activity, while oleuropein and hydroxytyrosol showed noteworthy potential. Secoiridoids contributed to the cyclooxygenase-2 inhibitory activity and antioxidant capacity. Compounds such as oleuropein, ligstroside and luteolin-7 -O- glucoside, may exert an important role in the ferric reducing antioxidant capacity. It should be also highlighted the role of hydroxytyrosol, hydroxycoumarins, and verbascoside concerning the antioxidant activity. This research provides valuable insights and confirms that specific compounds within OL extracts contribute to distinct anti-cholinergic, anti-inflammatory, and anti-oxidative effects. [ABSTRACT FROM AUTHOR]

Background: Osteoarthritis (OA) is a degenerative joint disease that causes a variety of adverse health effects. Considering the need to identify additional effective therapeutic options for OA therapy, we investigated the effect of co-injection of apigenin and synovial membrane-derived mesenchymal stem cells (SMMSCs) on OA in male rats' knee joints. Methods: The study was performed in 2019 at the Department of Pharmacology, Shiraz University of Medical Sciences, Shiraz, Iran. Anterior cruciate ligament transection (ACLT) was used to induce OA. For three weeks, male Sprague-Dawley rats (eight groups, n=6 each) were treated once-weekly with intra-articular injections of apigenin alone or in combination with SMMSC (three million cells), phosphate-buffered saline, or hyaluronic acid. After three months, the interleukin 1 beta (IL-1β), tumor necrosis factor-alpha (TNF- α), superoxide dismutase (SOD), and malondialdehyde (MDA) levels were measured in the cartilage homogenate. The expression of extracellular matrix (ECM) components including collagen 2a1, aggrecan, IL-1β, TNF-α, inducible nitric oxide synthase (iNOS), transcription factor SOX-9, and matrix metalloproteinases 3 and 13 were assessed using real-time polymerase chain reaction (RT-PCR) analysis. Radiological evaluation and histopathological assessment were used to evaluate the knees. Results: Levels of TNF-α (P=0.009), MDA (P0.001>), and IL-1β (P<0.001) decreased and the level of SOD increased (P=0.004) in the apigenin 0.3 µM with SMMSCs group. RT-PCR analysis indicated that IL-1β in the apigenin 0.3 µM with SMMSCs group reduced significantly (P>0.001). This group also exhibited increased expression levels of SOX-9, collagen 2a1, and aggrecan (P>0.001). Conclusion: Apigenin may have supplementary beneficial effects on cell therapy in a rat model of OA due to its possible effect on the reduction of oxidative stress, suppression of inflammation, and promotion of production of ECM components. [ABSTRACT FROM AUTHOR]

Lagotis brachystachya Maxim is a herb widely used in traditional Tibetan medicine. Our previous study indicated that total extracts from Lagotis brachystachya could lower uric acid levels. This study aimed to further elucidate the active components (luteolin, luteoloside and apigenin) isolated from Lagotis brachystachya and the underlying mechanism in vitro and in vivo. The results showed that treatment with luteolin and luteoloside reversed the reduction of organic anion transporter 1 (OAT1) levels, while apigenin attenuated the elevation of urate transporter 1 (URAT1) and glucose transporter 9 (GLUT9) levels in uric acid-treated HK-2 cells, which was consistent with the finding in the kidneys of potassium oxonate (PO)-induced mice. On the other hand, hepatic xanthine oxidase activity was inhibited by the components. In addition, all of these active components improved the morphology of the kidney in hyperuricemic mice. Moreover, molecular docking showed that luteolin, luteoloside and apigenin could bind Toll-like receptor 4 (TLR4) and NLR family pyrin domain containing 3 (NLRP3). Congruently, western blot analysis showed that the components inhibited TLR4/myeloid differentiation primary response 88 (MyD88)/NLRP3 signaling. In conclusion, these results indicated that luteolin, luteoloside and apigenin could attenuate hyperuricemia by decreasing the production and increasing the excretion of uric acid, which were mediated by inhibiting inflammatory signaling pathways. [ABSTRACT FROM AUTHOR]

Neuroinflammation is initiated by activation of the brain's innate immune system in response to an inflammatory challenge. Insufficient control of neuroinflammation leads to enhanced or prolonged pathology in various neurological conditions including multiple sclerosis and Alzheimer's disease. Nicotinamide adenine dinucleotide (NAD+) plays critical roles in cellular energy metabolism and calcium homeostasis. Our previous study demonstrated that deletion of CD38, which consumes NAD+, suppressed cuprizone-induced demyelination, neuroinflammation, and glial activation. However, it is still unknown whether CD38 directly affects neuroinflammation through regulating brain NAD+ level. In this study, we investigated the effect of CD38 deletion and inhibition and supplementation of NAD+ on lipopolysaccharide (LPS)-induced neuroinflammation in mice. Intracerebroventricular injection of LPS significantly increased CD38 expression especially in the hippocampus. Deletion of CD38 decreased LPS-induced inflammatory responses and glial activation. Pre-administration of apigenin, a flavonoid with CD38 inhibitory activity, or nicotinamide riboside (NR), an NAD+ precursor, increased NAD+ level, and significantly suppressed induction of cytokines and chemokines, glial activation and subsequent neurodegeneration after LPS administration. In cell culture, LPS-induced inflammatory responses were suppressed by treatment of primary astrocytes or microglia with apigenin, NAD+, NR or 78c, the latter a specific CD38 inhibitor. Finally, all these compounds suppressed NF-κB signaling pathway in microglia. These results suggest that CD38-mediated neuroinflammation is linked to NAD+ consumption and that boosting NAD+ by CD38 inhibition and NR supplementation directly suppress neuroinflammation in the brain. [ABSTRACT FROM AUTHOR]

Neuroinflammation is initiated by activation of the brain's innate immune system in response to an inflammatory challenge. Insufficient control of neuroinflammation leads to enhanced or prolonged pathology in various neurological conditions including multiple sclerosis and Alzheimer's disease. Nicotinamide adenine dinucleotide (NAD+) plays critical roles in cellular energy metabolism and calcium homeostasis. Our previous study demonstrated that deletion of CD38, which consumes NAD+, suppressed cuprizone‐induced demyelination, neuroinflammation, and glial activation. However, it is still unknown whether CD38 directly affects neuroinflammation through regulating brain NAD+ level. In this study, we investigated the effect of CD38 deletion and inhibition and supplementation of NAD+ on lipopolysaccharide (LPS)‐induced neuroinflammation in mice. Intracerebroventricular injection of LPS significantly increased CD38 expression especially in the hippocampus. Deletion of CD38 decreased LPS‐induced inflammatory responses and glial activation. Pre‐administration of apigenin, a flavonoid with CD38 inhibitory activity, or nicotinamide riboside (NR), an NAD+ precursor, increased NAD+ level, and significantly suppressed induction of cytokines and chemokines, glial activation and subsequent neurodegeneration after LPS administration. In cell culture, LPS‐induced inflammatory responses were suppressed by treatment of primary astrocytes or microglia with apigenin, NAD+, NR or 78c, the latter a specific CD38 inhibitor. Finally, all these compounds suppressed NF‐κB signaling pathway in microglia. These results suggest that CD38‐mediated neuroinflammation is linked to NAD+ consumption and that boosting NAD+ by CD38 inhibition and NR supplementation directly suppress neuroinflammation in the brain. [ABSTRACT FROM AUTHOR]

Psoriasis is an immune-mediated skin disease characterized by keratinocytes hyperproliferation, abnormal differentiation and inflammation. Therefore, this study aimed to investigate in-vitro and in-vivo anti-inflammatory and anti-proliferative activity to evaluate anti-psoriatic potential of apigenin. For in-vivo study, 5 % imiquimod cream was used to induce psoriasis-like skin inflammation in BALB/c mice to mimic human psoriatic conditions. PASI score, CosCam score, histopathology, immunohistochemistry, qRT-PCR, and ELISA were done to evaluate the anti-psoriatic potential of topically applied apigenin. For in-vitro studies, LPS-induced inflammation in RAW 264.7 was done, and qRT-PCR, ELISA, and immunofluorescence were conducted to evaluate the anti-inflammatory activity of apigenin. Migration and cell doubling assay in HaCaT cells were performed to assess the anti-proliferative effect of apigenin. Acute dermal toxicity profile of apigenin has also been done as per OECD guidelines. Results showed that apigenin significantly reduce the PASI and CosCam scores, ameliorate the deteriorating histopathology, and effectively downregulated the expression of CCR6, IL-17A, and NF-κB. Apigenin effectively downregulated the expression and secretion of pro-inflammatory cytokines through IL-23/IL-17/IL-22 axis. Apigenin suppressed nuclear translocation of NF-κB in LPS-induced RAW 264.7 cells. Cell migration and cell doubling assay in HaCaT cells showing the anti-proliferative potential of apigenin and it was found safe in acute dermal toxicity study. Apigenin was found effective against psoriasis in both in-vitro and in-vivo models suggesting apigenin as a potential candidate for the development of anti-psoriatic agent. [Display omitted] [ABSTRACT FROM AUTHOR]

Apigenin is one of the abundant flavonoids in fruits and vegetables of human diet with several demonstrated health benefits. The aim of the present study is to provide an overview of the current evidence regarding the effect of apigenin on different dermatological complications. Electronic databases including PubMed, Scopus, and Web of Science were searched to retrieve all papers assessing the dermatological effects of apigenin. Preclinical studies support beneficial effects of apigenin on UV-induced skin damage, vitiligo, dermatitis, wounds, skin aging, and some types of skin cancer. The compound mostly acts via inhibition of inflammation through suppression of pro-inflammatory cytokines and intracellular inflammatory mediators, as well as antioxidant properties such as improvement of endogenous antioxidant defense mechanisms. There are also some studies for the design and development of novel drug delivery systems for apigenin to improve its oral and topical bioavailability. Nevertheless, no clinical study has evaluated apigenin as a natural supplement for skin conditions. Considering the benefits of apigenin in preclinical models of dermatological disorders, as well as the acceptable safety of this compound, apigenin may be a future candidate to be used in dermatological disorders. Future clinical studies are needed to further confirm the safety and efficacy of apigenin in skin care products. [Display omitted] • Apigenin is an abundant flavonoid in human diet. • Preclinical studies show the benefits of apigenin in dermatological disorders. • Dermatological benefits of apigenin appear in both oral and topical administration. • Apigenin can be considered as a future cosmeceutical in skin care products. • Dietary apigenin-rich products can also be used to have a healthy skin. [ABSTRACT FROM AUTHOR]

Exposure to acrolein, one environmental and dietary pollutant, has been shown to cause inflammation. Here, we reported for the first time that acrolein aggravated lipopolysaccharide (LPS)-induced inflammation in Human umbilical vein endothelial cells (HUVEC) as evidenced by the further increased mRNA expression of three pro-inflammatory cytokines, including interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α). Acrolein also further increased the generation of reactive oxygen species (ROS) and decreased the activity of glutathione peroxidase (GSH-Px) in LPS-pretreated HUVEC. Moreover, acrolein treatment further increased the nucleotide oligomerization domain-like receptor protein 3 (NLRP3) and apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC) expression, caspase-1 cleavage, and downstream matures interleukin 18 (IL-18) and IL-1β level in LPS-pretreated HUVEC. Acrolein treatment also further increased the expressions of high-mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), and phospho–NF–κB P65 (P–P65) in the LPS pre-treated HUVEC. Thus, acrolein aggravated LPS-induced HUVEC inflammation through induction of oxidative stress, and activation of NLRP3 inflammasome and HMGB1/MYD88/NF-κB signaling pathway. In addition, apigenin and apigenin-7, 4′-O-dioctanoate attenuated acrolein-aggravated inflammation by targeting the above signaling pathways. Our findings could help to develop potential therapeutic strategies against acrolein-enhanced inflammation. [Display omitted] • Acrolein aggravated LPS-induced inflammation in HUVEC. • Acrolein increased ROS generation and decreased the GSH-Px activity. • Acrolein caused further activation of NLRP3 inflammasome. • Acrolein activated the HMGB1/TLR4/MyD88/NF-κB signaling pathway. • Apigenin-7, 4′-O-dioctanoate attenuated the acrolein-aggravated inflammation. [ABSTRACT FROM AUTHOR]