Effects Of Chrysin Research Articles

Cyclophosphamide-induced testicular injury: the role of chrysin in mitigating iron overload and ferroptosis.

This study evaluated the beneficial effects of chrysin against cyclophosphamide (CP)-induced testicular toxicity in rats across several parameters, including hormones, oxidative stress, inflammation, apoptosis, and protein expression. Rats were pretreated with oral doses of chrysin at 25, 50, or 100 mg/kg daily for 7 days. On the 8th day, all groups except controls received CP (200 mg/kg) injection. Chrysin doses continued for 7 more days. Hormones, oxidative stress markers, inflammatory cytokines, apoptosis regulators, and iron regulatory proteins were assessed. CP decreased testosterone, inhibin B, GSH, and GPx4 and increased FSH, cholesterol, MDA, IL-6, and BAX. It also drastically reduced TfR1, liprin, and IREB2. Chrysin dose-dependently counteracted these effects. The highest 100 mg/kg chrysin dose increased testosterone, inhibin B, GSH, GPx4, BCL2, TfR1, liprin, and IREB2 while decreasing FSH, cholesterol, MDA, IL-6, and BAX close to control levels. There were also significant incremental benefits for testosterone, inhibin B, and other parameters with higher chrysin doses. Chrysin dose-dependently attenuated CP-induced hormonal dysfunction, oxidative stress, inflammation, apoptosis, and iron-regulatory protein suppression. The maximum dose showed the most optimal protective effects in restoring the testicular toxicity markers. These results validate the promising spermatoprotective properties of chrysin against chemotherapeutic germ cell damage.

Effect of Chrysin and Chrysin Nanocrystals on Chlorpyrifos-Induced Dysfunction of the Hypothalamic-Pituitary-Testicular Axis in Rats

The escalating global concerns regarding reproductive health underscore the urgency of investigating the impact of environmental pollutants on fertility. This study aims to focus on Chlorpyrifos (CPF), a widely-used organophosphate insecticide, and explores its adverse influence on the hypothalamic-pituitary-testicular axis in Wistar male rats. This study explores the potential protective effects of chrysin nanocrystal (CHN), a flavonoid with known antioxidant and anti-inflammatory properties, against CPF-induced impairments in male Wistar rats. Chrysin nanocrystals were prepared using a solvent precipitation method. Six sets of male Wistar rats were subjected to 30 days of treatment, comprising a control group, a group treated solely with CPF, groups treated with CHN at doses of 5 mg/kg and 10 mg/kg, and groups co-treated with CPF and CHN. Serum levels of reproductive hormones, enzyme biomarkers of testicular function, oxidative stress, and inflammatory biomarkers were assessed. Additionally, histological examinations were conducted on the hypothalamus, testes, and epididymis. CHN exhibited antioxidant and anti-inflammatory properties, effectively counteracting CPF-induced reductions in Luteinizing Hormone (LH), serum testosterone, Follicle-Stimulating Hormone (FSH), and testicular enzyme biomarkers. Moreover, CHN enhanced antioxidant defenses, as evidenced by decreased malondialdehyde (MDA) and increased glutathione (GSH) levels in the hypothalamus, and testes, epididymis. Inflammatory markers, including nitric oxide (NO), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), were significantly reduced in CHN co-treated groups compared to the CPF-only group. Histopathological analyses confirmed the protective effects of CHN on tissue integrity. Chrysin nanocrystal demonstrated promising potential in mitigating CPF-induced reproductive deficits in male rats through its anti-inflammatory and antioxidant properties. This study provides valuable insights into therapeutic interventions against environmental toxin-induced reproductive toxicity, emphasizing the potential of chrysin nanocrystals as a protective agent in the context of CPF exposure.

Induction of immunogenic cell death and enhancement of the radiation-induced immunogenicity by chrysin in melanoma cancer cells

Chrysin is a natural flavonoid with anti-cancer effects. Despite its beneficial effects, little information is available regarding its immunogenic cell death (ICD) properties. In this work, we hypothesized that chrysin can potentiate radiotherapy(RT)-induced immunogenicity in melanoma cell line (B16-F10). We examined the effects of chrysin alone and in combination with radiation on ICD induction in B16-F10 cells. Cell viability was assessed using an MTT assay. Cell apoptosis and calreticulin (CRT) exposure were determined using flow cytometry. Western blotting and ELISA assay were employed to examine changes in protein expression. Combination therapy exhibited a synergistic effect, with an optimum combination index of 0.66. The synergistic anti-cancer effect correlated with increased cell apoptosis in cancer cells. Compared to the untreated control, chrysin alone and in combination with RT induced higher levels of DAMPs, such as CRT, HSP70, HMGB1, and ATP. The protein expression of p-STAT3/STAT3 and PD-L1 was reduced in B16-F10 cells exposed to chrysin alone and in combination with RT. Conditioned media from B16-F10 cells exposed to mono-and combination treatments elicited IL-12 secretion in dendritic cells (DCs), inducing a Th1 response. Our findings revealed that chrysin could induce ICD and intensify the RT-induced immunogenicity.

Chrysin attenuates epithelial prostatic hyperplasia in the ventral prostate of spontaneously hypertensive rats.

The aim of this study was to evaluate the effects of chrysin on the ventral prostate of spontaneously hypertensive rats (SHR). Ten-week-old male Wistar and SHR rats received 100 mg/kg/day of chrysin (TW and TSHR) or 200 µL/day of the dilution vehicle (CW and CSHR) for 70 days. After the treatment, the animals were euthanized and the prostates were dissected out, fixed, and processed for further morphological, immunohistochemical, and biochemical analyses. Blood was collected for serological analysis. Chrysin did not interfere with the blood pressure. Morphologically, the epithelial height increased in TW and decreased in TSHR. Stereology showed an increase in the epithelial and stromal relative frequency, and a decrease in the lumen of TW, whereas the epithelium in TSHR was reduced. Normal alveoli decreased, and hyperplastic alveoli had an increment in TW, whereas in TSHR normal alveoli increased and intense hyperplasia decreased. The secretion area was reduced in TW. Immunohistochemical analysis showed a smaller number of PCNA-positive cells in TW. Finally, the biochemical analysis showed a reduction in malondialdehyde, carbonylated proteins, superoxide dismutase, and catalase in TW and TSHR. We concluded that the chrysin effect is dependent on the context in which this flavonoid is employed. In normal conditions, the anabolic potential of the chrysin was favored, disrupting the morphology of the prostate. However, when used in animals predisposed to develop hyperplasia, this flavonoid attenuates the hyperplastic status, improving the morphology of the gland.

Flavonoid chrysin activates both TrkB and FGFR1 receptors while upregulates their endogenous ligands such as brain derived neurotrophic factor to promote human neurogenesis.

Neurogenesis is the process of generating new neurons from neural stem cells (NSCs) and plays a crucial role in neurological diseases. The process involves a series of steps, including NSC proliferation, migration and differentiation, which are regulated by multiple pathways such as neurotrophic Trk and fibroblast growth factor receptors (FGFR) signalling. Despite the discovery of numerous compounds capable of modulating individual stages of neurogenesis, it remains challenging to identify an agent that can regulate multiple cellular processes of neurogenesis. Here, through screening of bioactive compounds in dietary functional foods, we identified a flavonoid chrysin that not only enhanced the human NSCs proliferation but also facilitated neuronal differentiation and neurite outgrowth. Further mechanistic study revealed the effect of chrysin was attenuated by inhibition of neurotrophic tropomyosin receptor kinase-B (TrkB) receptor. Consistently, chrysin activated TrkB and downstream ERK1/2 and AKT. Intriguingly, we found that the effect of chrysin was also reduced by FGFR1 blockade. Moreover, extended treatment of chrysin enhanced levels of brain-derived neurotrophic factor, as well as FGF1 and FGF8. Finally, chrysin was found to promote neurogenesis in human cerebral organoids by increasing the organoid expansion and folding, which was also mediated by TrkB and FGFR1 signalling. To conclude, our study indicates that activating both TrkB and FGFR1 signalling could be a promising avenue for therapeutic interventions in neurological diseases, and chrysin appears to be a potential candidate for the development of such treatments.

Chrysin downregulates the expression of ADAMTS-4 in foam cells.

Chrysin, a polyphenolic compound, possesses antioxidant and anti-inflammatory properties. In this study, we investigated the effect of chrysin on the expression of A disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4), a protease enzyme involved in degrading extracellular matrix associated with atherosclerosis. We have studied the cell viability by MTT assay and foam cell formation by oil red O staining. The mRNA and protein expression of ADAMTS-4 was studied using quantitative polymerase chain reaction (qPCR) and Western blotting, respectively. Our study showed that chrysin significantly downregulates the expression of ADAMTS-4 in foam cells. Chrysin's ability to downregulate the expression of ADAMTS-4, a protease involved in degrading the extracellular matrix, bestows upon it a new therapeutic potential for managing atherosclerosis.

Chrysin attenuates hyperglycemia associated with hepatorenal and glycoprotein abnormalities via regulation of glucose metabolism in HFD/STZ- induced diabetic rats

BackgroundFlavonoids like chyrsin, which are abundant in plant extracts, honey, and bee propolis, have antiviral, anti-cancer, anti-bacterial, anti-inflammatory, anti-allergic, anti-mutagenic, anti-anxiolytic, and other therapeutic uses. However, no research has been published on how chrysin protects rats against HFD/STZ- induced changes to the glycoprotein moiety via controlling the metabolism of glucose. MethodsFor two weeks, albino male wistar rats were fed a high-fat diet in order to develop diabetes. Upon two weeks, a low dosage of streptozotocin (35 mg/kg, diluted in 0.1 M sodium citrate buffer, pH 4.5) was administered into the animals after they had been fasted for the whole night. Blood glucose, insulin, hepatic, and renal indicators were analyzed using commercially available diagnostic kits, and other parameters were ascertained biochemically. ResultsFor 30 days, high-fat diet- and streptozotocin-induced diabetic rats were given 40 mg/kg b.w./day of chrysin, which significantly reduced blood glucose, homeostatic model assessment of insulin resistance, glycogen phospharylase, hepatic and renal markers, and increased insulin, glycogen content, and glycogen synthase levels. ConclusionHowever, the altered activity of the glycoprotein components and the carbohydrate metabolic enzymes was restored upon chrysin administration. On several criteria, the chrysin's effect was similar to that of metformin. Chrysin is therefore a potential antidiabetic agent.

Study of the Central Injection Effects of Chrysin on Behavioral and Intra Hypothalamic Gene Expression Levels of CRH and CGRP in Male Rats

Background: Chrysin is a natural flavonoid with several demonstrated neuro-pharmacological effects in brain areas related to anxiety. However, the intra-hypothalamic molecular mechanisms underlying the anxiolytic effects of chrysin remain unclear. Objectives: The current study revealed the effects of chrysin on hypothalamic corticotrophin-releasing hormone (CRH) and calcitonin gene-related peptide (CGRP) gene expression levels in a rat model of stress. Methods: Thirty male Wistar rats weighing 200 ± 10 g were divided into six groups for this investigation. Acute restraint stress was induced in the animals for 2 hours. Intact or stress-induced rats received 20 or 40 µg of chrysin via the third cerebral ventricle, respectively. Open-field and forced swimming tests were performed to evaluate stress-related behaviors. Hypothalamic samples were then removed, and real-time polymerase chain reaction (PCR) was used to measure relative gene expression. Results: The results showed that in the rats receiving chrysin, CRH and CGRP gene expression levels were significantly decreased compared to the stress group. Additionally, chrysin injection reduced anxiogenic behaviors. Conclusions: Chrysin decreased the expression of hypothalamic CRH and CGRP genes in stressed rats.

The possible protective effects of Chrysin on cerebral and cerebellar cortices of adult male albino rats exposed to induced hyperlipidemia ( Histological and Immunohistochemical study)

The possible protective effects of Chrysin on cerebral and cerebellar cortices of adult male albino rats exposed to induced hyperlipidemia ( Histological and Immunohistochemical study)

The ameliorative effects of chrysin on bortezomib-induced nephrotoxicity in rats: Reduces oxidative stress, endoplasmic reticulum stress, inflammation damage, apoptotic and autophagic death

AimBortezomib is a proteasome inhibitor antineoplastic agent that was the first to be approved for cancer treatment. One of bortezomib's most prominent dose-limiting effects is nephrotoxicity; the underlying mechanism is believed to be oxidative stress. Chrysin is a compound found actively in honey and many plant species and stands out with its antioxidant properties. The present study aimed to determine the ameliorative effects of chrysin in bortezomib-induced nephrotoxicity. Material-methodThirty-five male Wistar rats were divided into control, BTZ, CHR, BTZ + CHR25, and BTZ + CHR50. Biochemical, molecular, Western blot, and histological methods analyzed renal function indicators, oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, and damage pathways. ResultsChrysin decreased oxidative stress by reducing oxidants (MDA) and increasing antioxidants (SOD, CAT, Gpx, GSH, Nrf-2, HO-1, NQO1). Chrysin reduced endoplasmic reticulum stress by decreasing ATF-6, PERK, IRE1, and GRP-78 levels. Chrysin reduced inflammation damage by inhibiting the NF-κB pathway. Chrysin exhibited protective properties against apoptotic damage by decreasing Bax and Caspase-3 levels and increasing Bcl-2 levels. In addition, chrysin improved renal function and structural integrity and exhibited healing properties against toxic damage in tissue structure. ConclusionOverall, chrysin exhibited an ameliorative effect against bortezomib-induced nephrotoxicity.

Synergistic effect of chrysin and kaempferol in ameliorating Cerebral Ischemic Reperfusion injury in rat by controlling expression of proinflammatory mediators NF-κB and STAT3

ABSTRACT Objectives The two flavonoids kaempferol and chrysin are known to possess anti-inflammatory and antioxidant activities. In addition, these two flavonoids were reported to display synergistic effects against inflammation. The present study aims to provide an analysis of the combined effects of kaempferol and chrysin on ischemic rat brain induced by endothelin-1. Methods The neurological deficit score and infarct area of the brain were determined post drug treatment. Histopathological sections displayed the morphological changes in the brain tissue. The brain tissues were processed for assessing the antioxidant and anti-inflammatory activity by measuring superoxide dismutase activity, catalase activity, level of reduced glutathione, brain malondialdehyde, and amount of calcium. The expression level of inflammatory molecules was analyzed by western blotting and immunohistochemistry. Results The infarct area, neurological score and NF-κB and STAT3 expression levels were significantly reduced. Discussion The analysis of neuroprotective synergistic activity of kaempferol and chrysin indicated the therapeutic potential of the combination in alleviating cerebral ischemia by controlling expression of proinflammatory mediators.

Advancements and recent explorations of anti-cancer activity of chrysin: from molecular targets to therapeutic perspective.

In recent times, there have been notable advancements in comprehending the potential anti-cancer effects of chrysin (CH), a naturally occurring flavonoid compound found abundantly in various plant sources like honey, propolis, and certain fruits and vegetables. This active compound has garnered significant attention due to its promising therapeutic qualities and minimal toxicity. CH's ability to combat cancer arises from its multifaceted mechanisms of action, including the initiation of apoptosis and the inhibition of proliferation, angiogenesis, metastasis, and cell cycle progression. CH also displays potent antioxidant and anti-inflammatory properties, effectively counteracting the harmful molecules that contribute to DNA damage and the development of cancer. Furthermore, CH has exhibited the potential to sensitize cancer cells to traditional chemotherapy and radiotherapy, amplifying the effectiveness of these treatments while reducing their negative impact on healthy cells. Hence, in this current review, the composition, chemistry, mechanisms of action, safety concerns of CH, along with the feasibility of its nanoformulations. To conclude, the recent investigations into CH's anti-cancer effects present a compelling glimpse into the potential of this natural compound as a complementary therapeutic element in the array of anti-cancer approaches, providing a safer and more comprehensive method of combating this devastating ailment.

Effect of chrysin on oxidative stress, biochemical, and inflammatory alterations in Wistar albino rats exposed to cypermethrin

Effect of chrysin on oxidative stress, biochemical, and inflammatory alterations in Wistar albino rats exposed to cypermethrin

Effects of Chrysin and Chrysin-7-sulfate on Ochratoxin A-Albumin Interactions and on the Plasma and Kidney Levels of the Mycotoxin in Rats.

The nephrotoxic mycotoxin ochratoxin A (OTA) is a common food contaminant. OTA binds to the Sudlow's Site I region of serum albumin with very high affinity, resulting in its slow elimination. The displacement of OTA from albumin may be beneficial due to the faster excretion of the mycotoxin, while it may also lead to the increased tissue uptake of OTA. Furthermore, it is challenging to displace the mycotoxin from albumin even with high-affinity Site I ligands. In this study, we tested the impacts of Site I and Heme site ligands on OTA-albumin interactions by applying fluorescence spectroscopic, ultracentrifugation, and modeling studies. Chrysin-7-sulfate (C7S) strongly displaced OTA from both human and rat albumins; therefore, the impacts of C7S (single intravenous administration) and the parent flavonoid chrysin (repeated peroral treatment) were examined on the plasma and kidney levels of OTA in rats. Chrysin barely influenced the concentrations of mycotoxin in plasma and kidneys. In the first few hours, C7S significantly decreased the plasma levels of OTA compared to the control animals; while after 24 h, only minor differences were noticed. Our study highlights the superior displacing ability of C7S vs OTA regarding human and rat albumins.

Chrysin inhibits ferroptosis of cerebral ischemia/reperfusion injury via regulating HIF-1α/CP loop

Chrysin is a natural flavonoid with powerful neuroprotective capacity. Cerebral ischemia/reperfusion injury (CIRI) is associated with oxidative stress and ferroptosis. Hypoxia-inducible factor 1α (HIF-1α) and ceruloplasmin (CP) are the critical targets for oxidation reactions and iron transport. But the regulatory mechanism between them is still unclear. Transient middle cerebral artery occlusion (tMCAO) model in rats and oxygen and glucose deprivation/re-oxygenation (OGD/R) model in PC12 cells were applied. Pathological tissue staining and biochemical kit were used to evaluate the effect of chrysin. The relationship between HIF-1α and CP was verified by transcriptomics, qRT-PCR and Western blot. In CIRI, HIF-1α/CP loop was discovered to be the regulatory pathway of ferroptosis. CIRI led to activation and nuclear translocation of HIF-1α, which promoted CP transcription and translation, and downstream ferroptosis. Inhibition of HIF-1α had opposite effect on CP and ferroptosis regulation. Overexpression of CP increased the expression of HIF-1α, nevertheless, inhibited the nuclear translocation of HIF-1α and alleviated CIRI. Silencing CP promoted HIF-1α elevation in nucleus and aggravated CIRI. Mechanistically, chrysin restrained HIF-1α nuclear translocation, thereby inhibiting CP transcription and translation, which in turn reduced downstream HIF-1α expression and mitigated ferroptosis in CIRI. Our results highlight chrysin restrains ferroptosis in CIRI through HIF-1α/CP loop.

The Effect of Chrysin on the Distribution of Extracellular Matrix Proteins around Leydig Cells under Heat Stress Injury

Objective. In the testicular tissue stroma, matrix proteins such as laminin and fibronectin play a critical role in transmitting signals under normal and stressful conditions to Leydig cells. Heat stress is considered one of the stressful conditions in the testicular tissue. This study has investigated the protective effects of chrysin on the distribution of laminin and fibronectin around Leydig cells under heat stress. Methods. Rats were divided into four groups, including sham (A), heat stress (B), heat stress with chrysin treatment (50 mg/kg) (C), and heat stress with chrysin treatment (75 mg/kg) (D). At the end of the treatment period, on the 21st day, testosterone serum levels were evaluated, and the testes were also assessed to determine the changes in gene expression and distribution of laminin, fibronectin, and caspase-3 proteins. Results. Exposure to heat stress in Group B resulted in increased levels of caspase-3, decreased activity, height, and diameter of seminiferous tubules, and altered distribution of laminin and fibronectin proteins around the Leydig cells when compared to the sham group (p<0.05). Treatment with chrysin 75 resulted in a significant decrease in caspase-3 levels, improved testosterone levels, and increased distribution of laminin and fibronectin around Leydig cells compared to group B (p<0.05). In addition, the group treated with chrysin 75 showed improved seminiferous histological activity markers in comparison to group B (p<0.05). Conclusion. Following heat stress, concurrent with disrupted steroidogenesis, an evident change happens in the distribution pattern of the extracellular matrix (ECM) proteins of the testis, which may indicate the transmission of stress signals from the ECM to the Leydig cells. Treatment of chrysin in 75 mg/kg dose can reduce the damage caused by heat stress on the ECM and Leydig cells.

The Influences of Chrysin on Stress-Induced Changes of Melanin-Concentrating Hormone and Orexin Gene Expression in Rats

Introduction: Chrysin is a bioactive component of herbal medicines such as Passiflora incarnate, Passiflora caerulea, and Oroxylum indicum. Although evidence has demonstrated the neuroprotective, anti-inflammatory, and pain-relieving effects of chrysin, the intra-hypothalamic molecular mechanisms underlying the anxiolytic effects of chrysin are still unclear. This study aimed to explore the effects of chrysin on hypothalamic orexin and melanin-concentrating hormone (MCH) gene expression in a rat model of stress. Methods: Twenty male Wistar rats (200±10 g) were segregated into four groups (n=5). For the induction of stress, the animals were placed in the restraint cage for 2 hours. The intact and stressed groups received saline. Thirty minutes before the induction of stress, chrysin was injected into the other two groups of the stress model at a dosage of 20 or 40 µg via the third cerebral ventricle. Hypothalamic samples were removed and frozen, and the relative gene expression of orexin and MCH was measured using the real-time polymerase chain reaction technique. Results: The induction of stress significantly increased mRNA levels of orexin and MCH compared to the control rats. The mRNA levels of MCH and orexin significantly declined in rats receiving chrysin compared to the stress group. Conclusion: The inhibition of the hypothalamic MCH and orexin neuronal circuits may be involved in the preventive effects of chrysin against stressful situations. Chrysin may be a potential target to manage anxiogenic behaviors due to the down-regulation of MCH and orexin gene expression upstream the hypothalamic corticotropin-releasing hormone.

Investigation of the Protective Effects of Chrysin Against Paclitaxel-Induced Oxidative Stress and Apoptosis in Human Neuronal SH-SY5Y Cells

In this study, the potential protective effects of chrysin, an important flavonoid, against paclitaxel-induced cell toxicity in the SH-SY5Y nerve cell line as an in vitro model, were investigated by cell viability analysis, lipid peroxidation analysis and quantitative simultaneous PCR methods. In the study, firstly, paclitaxel and chrysin were applied to the SH-SY5Y cell line at different concentrations in the range of 0-30 µM, and the results showed that 15 and 30 µM paclitaxel reduced cell viability, and 500 and 1000 µM chrysin application reduced these effects. In addition, chrysin application has been shown to significantly reduce malondialdehyde levels in paclitaxel-induced cells. The study also examined the effects of paclitaxel and chrysin application on apoptotic and antiapoptotic genes, mostly located in the intrinsic pathway, and showed that chrysin significantly reduced the levels of caspase 10, caspase 8, caspase 6, p53 and NFKB, and increased the Bcl-2 level compared to the paclitaxel-treated group. The results of this study suggest that chrysin's suppression of oxidative stress and apoptotic cell death may be an effective strategy for the treatment of paclitaxel-induced SH-SY5Y cytotoxicity.

Chrysin, The Flavonoid Molecule of Antioxidant Interest

AbstractChrysin, the natural bioactive flavone compound, has been identified in several edible materials such as honey, propolis, and passionflower with numerous biological potentials and pharmaceutical effects including antitumor, anti‐inflammatory, antiviral and antioxidant. The compound has been reported to have lower in vitro antioxidant activity compared to other flavone‐based structures such as quercetin, luteolin, and myricetin, which is mostly attributed to the higher hydroxylation and the presence of conjugated en‐diol structures in these flavonoids and the lack of these structural features in chrysin. On the contrary to the in vitro antioxidant effect of chrysin, the compound has exerted remarkable in vivo antioxidant activities in several models related to the liver, brain, heart, kidneys, and other soft tissues. The current review includes a discussion of the in vivo and in vitro antioxidant activity of chrysin compared to other common flavonoids. The study also covers subjects linked to chrysin antioxidants, such as its metabolism, bioavailability, and current formulations that aim to increase chrysin antioxidant impact and overcome its low bioavailability.

Chrysin Effect Against Gastric Cancer: Focus on its Molecular Mechanisms.

Gastric cancer is one of the most prevalent cancers in the world. Various therapeutic modalities have been used for its treatment, but all exhibit severe side effects, establishing the need for novel approaches. Chrysin is a phytomedicine compound belonging to the flavonoid group. It is found in honey and many plants. Its antitumor effects have been documented against gastric cancer cell lines in vitro, establishing its effects are mediated via different pathways and the expression of miRNA. In this review, we summarize the available literature on chrysin and its effects on gastric cancer, focusing on the cellular mechanisms it targets.