Biological Activities of Crude Grape Tendril Extract Against Oxidative Stress,Inflammation,and Allergy

Abstract

Objective

This study investigates the potential of grape tendril extracts (G.T.) derived from Shine Muscat variety in mitigating oxidative stress, inflammation, and allergic reactions, focusing on stress granule (SG) dynamics, inflammatory pathways, and mast cell responses.

Methods

G.T. was extracted using 50% ethanol and assessed for antioxidant activity via ABTS radical scavenging assay. Its anti-inflammatory effects were evaluated in RAW 264.7 cells by measuring inflammatory cytokine expression (TNF-α, IL-6, IL-1β) using qRT-PCR and NF-κB pathway components by immunoblotting. SG formation was visualized in AGS cells under arsenite-induced oxidative stress through G3BP1 immunofluorescence staining. Anti-allergic properties were determined through β-hexosaminidase release assay in RBL-2H3 mast cells.

Results

G.T. demonstrated potent antioxidant activity with 88% radical scavenging at 4 mg/mL. It significantly suppressed LPS-induced pro-inflammatory cytokine expression and IκBα phosphorylation in RAW 264.7 cells. Under oxidative stress, G.T. (0.5 mg/mL) reduced both the number of SG-positive cells and SGs per cell in AGS cells. Moreover, G.T. inhibited compound 48/80-induced β-hexosaminidase release in RBL-2H3 cells dose-dependently.

Conclusions

These findings establish G.T. as a promising natural therapeutic agent with significant antioxidant, anti-inflammatory, and anti-allergic properties. The demonstrated effects on SG formation provide new insights into its cellular protective mechanisms.

Introduction

Grape tendrils, the thread-like structures that support climbing grapevines, have historically been viewed as agricultural byproducts with minimal utility.^1-3 However, recent research has revealed that these tendrils are a rich source of bioactive compounds with potential therapeutic applications.^4-10 Notably, grape tendril extracts have garnered attention for their antioxidant and anti-inflammatory properties, which could be beneficial in addressing oxidative stress and inflammation-related disorders.^11-18 While these initial findings are promising, the comprehensive biological activities and underlying mechanisms of grape tendril extracts remain largely unexplored.

Oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) and the body's antioxidant defenses, leads to cellular damage and the activation of inflammatory pathways.^19,20 Given oxidative stress can trigger the formation of stress granules (SGs), dynamic complexs of proteins and RNAs aggregating in response to cellular stress.^21-23 These granules play a crucial role in regulating gene expression during stress conditions, and their dysregulation has been implicated in the pathogenesis of various diseases, including cancer and neurodegenerative disorders.^24-27 Thus, targeting oxidative stress and SG dynamics represents a promising approach to mitigating these adverse effects.

Inflammation, while a protective biological response, can become harmful when chronic or excessive. The NF-κB signaling pathway is central to the inflammatory response, mediating the expression of key pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β.^28-30 Overactivation of inflammation is associated with various inflammatory diseases, making it a critical target for anti-inflammatory interventions.^31,32 In recent years, various plant-derived extracts have been reported to exert anti-inflammatory effects by modulating NF-κB activity. Natural compounds such as curcumin, resveratrol, and epigallocatechin gallate (EGCG) have been shown to suppress NF-κB signaling and thereby reduce the expression of pro-inflammatory cytokines.^33,34 Tendrils, a byproduct of grape tendrils, also contain a variety of bioactive compounds and may possess anti-inflammatory properties.^35,36 However, the effects of grape tendrils extract on the NF-κB signaling pathway and its underlying mechanisms remain largely unclear. Therefore, this study investigates how grape tendril extract influences NF-κB signaling and explores its potential anti-inflammatory properties. In addition to oxidative stress and inflammation, allergic reactions are another area of concern where grape tendril extracts could offer therapeutic benefits. Allergic responses often involve mast cell degranulation, a process that releases mediators like β-hexosaminidase, contributing to allergic symptoms.^37-39

We hypothesized that grape tendril extracts, rich in polyphenolic compounds, could effectively reduce ROS levels, inhibit SG formation, and suppress inflammatory responses by modulating the NF-κB pathway. By inhibiting mast cell degranulation, these extracts could potentially serve as natural anti-allergic agents. This study aimed to validate these properties through a series of in vitro experiments, thereby highlighting grape tendril extracts’ potential as a natural source for developing therapeutic agents against oxidative stress, inflammation, and allergies. Understanding these mechanisms could establish grape tendrils as a valuable resource for therapeutic applications, transforming an agricultural byproduct into a beneficial health resource.

Materials and Methods

Preparation of Grape Tendrils Extract

The grape tendrils were harvested from Shine Muscat (Vitis labruscana Baily x Vitis vinifera vitis vinifera L.) cultivar. The grape tendrils were placed in a beaker containing 50% ethanol (w/v) and extraction was carried out at 50 °C, 1 atm for 6 h. The extracts were filtered through filter paper (Filter paper Qual., General F1093, 110 mm) and a concentrated solution was obtained using a Rotavapor^® R-100. The concentrated solution was hot air dried at 50 °C and the extract powder was ground and used as a sample.^1,40 The extraction yield was calculated to be 12.5% (w/w)

Folin-Ciocalteu Assay

The total phenolic content (TPC) of G.T. extract was determined using the modified Folin–Ciocalteu assay in a 96-well microplate, as described by Kurniawan et al ⁴¹ Briefly, 20 μL of extract (1 mg/mL) or gallic acid standard (0-80 μg/mL, SIGMA, St. Louis, MO, USA) was mixed with 100 μL of 1:10 diluted Folin–Ciocalteu reagent (Junsei Chemical Co., Ltd, Tokyo, Japan). After 5 min in the dark at room temperature, 80 μL of sodium carbonate (7.5%, SIGMA) was added, and the mixture was incubated for 30 min in the dark. Absorbance was measured at 760 nm.

High-performance Liquid Chromatography

The analysis was performed using a zorbax Eclipse XDB-C18 column (50 × 4.6 mm, 5 μm; Santa Clara), with an Agilent 1260 Infinity LC (Santa Clara) instrument. The mobile phase consisted of solvent A (deionized water: acetic acid, 99.9: 0.1, v/v) and solvent B (acetonitrile), with A flow rate of 1 mL/min. ⁴² A sample volume of 25 μL was injected onto the column, and separation was achieved using the following gradient program: 0 min, 100% B; 1 min, 10% B; 15 min, 100% B; and 18 min, 10% B. The detection wavelength was set at 306 nm, and the total run time was 18 min.

Cell Culture and Chemicals

Human aneuploid keratinocytes HaCaT, murine melanoma B16F10 cells (ATCC, Manassas, VA, USA), murine macrophage RAW 264.7 (ATCC), murine basophilic leukemia mast cells RBL-2H3 (ATCC), and human stomach AGS cells (ATCC) were cultured in DMEM medium (Welgene, Gyeongsangbuk-do, Korea) with 10% heat-inactivated fetal bovine serum (Gibco, MA, USA), and 1% penicillin and streptomycin at 37 °C in a humidified atmosphere of 5% CO₂.

Free Radical Scavenging Assay

The antioxidant activity of G.T. was measured using the ABTS (2,2′-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid) radical scavenging assay. ⁴³ The ABTS assay was performed by mixing a 2.4 mM solution of potassium persulfate (SIGMA) with 7 mM of ABTS⁺ (SIGMA) and reacting for 24 h in the quenched state to the ABTS radical state. The ABTS radical state was then diluted with water to obtain an absorbance of 0.7 ± 0.01 units at 650 nm. In a 96-well plate, 20 μL of G.T. was added for each concentration, followed by 80 μL of ABTS⁺ radical agent, and the reaction was carried out for 4 min, and the absorbance was measured at 650 nm using a microplate reader (Molecular Devices EXax Plus, San Jose, CA, USA). The antioxidant potency of G.T. as a percentage of the vehicle control was calculated as follows: ABTS⁺ radical scavenging activity (%) = [1 − (Abs_sample − Abs_blank of sample)/Abs_control] × 100, where Abs_control is the absorbance of ABTS⁺ radical solution diluted in water, Abs_sample is the absorbance of ABTS⁺ radical solution mixed with G.T., and Abs_blank of sample is the absorbance of water mixed with G.T.

Cell Viability Assay

The cytotoxicity of G.T. on AGS_G3BP1_KI, HDF, HaCaT, and B16F10 cells were measured using the CellTiter 96^® AQueous One Solution cell proliferation assay (Promega, Madison, WI, USA). Cells were seeded (30,000 cells/well) in 96-well plates and incubated for 24 h, then culture medium containing G.T. was added to the plates in each well and incubated for 36 h. 20 μL of MTS reagent was added and absorbance was measured at 490 nm using a microplate reader (Molecular Devices EXax Plus). ⁴⁴ The following formula was used for cell viability calculation: Cell viability (%) = {(Abs_sample − Abs_blank)/(Abs_control − Abs_blank)} × 100, where Abs is the absorbance for the wavelength of sample.

RNA Extraction and Quantitative Reverse Transcription-polymerase Chain Reaction (qRT-PCR) Analysis

RAW 264.7 cells were seeded at 2 × 10⁵ cells/well in 6-well culture dishes and incubated for 24 h. They were then treated with G.T. 0.5, 1 mg/mL for 24 h and LPS was added to the medium at a final concentration of 1 μg/mL, followed by incubation for 6 h. ⁴⁵ The culture medium was removed completely, the cells were washed with cold PBS and lysed with 1 mL of RiboEx (GeneAll, Seoul, Korea), and RNA was extracted using the Hybrid-R RNA purification kit (GeneAll). For cDNA synthesis, 1 μg of total RNA was combined with 1 μL of Random Hexamer (100 pmol/μL), 1 μL of dNTP mix (10 mM), and then adjusted to a total volume of 10 μL with DEPC-treated water. The mixture was reacted at 65 °C for 5 min and immediately cooled on ice. Thereafter, 1 μL RNase inhibitor (Enzynomics, Chungcheongnam-do, Korea), 1 μL M-MLV reverse transcriptase (Promega), 4 μL 5X MMLB RT reaction buffer (Promega), and 4 μL of DEPC-treated water were added to each RNA sample, and the mixture was incubated at RT for 10 min, followed by 50 °C, 1 h to complete the synthesis. The mRNA expression levels of inflammatory cytokines were comparatively analyzed using qRT-PCR. qRT-PCR was performed using AriaMx (Agilent, Santa Clara, CA, USA) according to the conditions: 5 μL of cDNA contained 10 μL of 2X Prime Q-master Mix (GENET BIO, Chungcheongnam-do, Korea), 1.5 μL of forward primer (10 pmol/μL), 1.5 μL of reverse primer (10 pmol/μL), and 2 μL of nuclease free water. The conditions were as follows: 40 cycles of denaturation at 95 °C for 20 s, annealing at 58 °C for 20 s, and elongation at 72 °C for 20 s. β-Actin was used as the internal standard. The following primers were used: TNF-a, 5′-AGG GTC TGG GCC ATA GAA CT-3′ and 5′-CCA CCA CGC TCT TCT GTC TAC-3′; IL-6, 5′-GTC CTT CAG AGA GAT ACA GAA ACT-3′ and 5′- AGC TTA TCT GTT AGG AGA GCA TTG-3′; IL-1b, 5′- AGG TCA AAG GTT TGG AAG CA-3′ and 5′- TGA AGC AGC TAT GGC AAC TG-3′; β-actin, 5′-TCA CCC ACA CTG TGC CCA TCT ACG-3′ and 5′-CAG CGG AAC CGC TCA TTG CCA ATG-3′.

Immunoblot Analysis

RAW 264.7 cells were seeded in 6-well culture plates at 1 × 10⁵ cells/well and incubated for 24 h. Medium containing G.T. was added, and the plates were incubated for 24 h. LPS was added to the medium at a final concentration of 1 μg/mL and incubated for 1 h. To prepare protein samples, all medium was removed and cells were washed with cold PBS, and nuclear/cytoplasmic proteins and whole cell lysates were separated using M-PER buffer (Thermo Fisher Scientific, Waltham, MA, USA). The protease inhibitor cocktail (Roche Applied Science, Schlieren, Switzerland) was added at this time. Protein samples were sonicated and centrifuged at 16,000xg for 10 min. The supernatant was transferred to a new tube and the protein concentration was measured with BCA reagent (Thermo Fisher Scientific). Proteins were separated using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and transferred to a nitrocellulose membrane (0.45 μm, Merck Millipore, Burlington, MA, USA). The membrane was blocked in PBST containing 5% skimmed milk (Rockland Immunochemicals, Limerick, PA, USA) for 1 h and incubated with anti-phospho-IκBα (9246S, 1:500, Cell Signaling Technology, Danvers, MA, USA), anti-IκBα (L35A5, 1:500, Cell Signaling Technology), and anti-α-Tubulin (T9026, 1:1000, Sigma) antibodies diluted in blocking buffer for 16 h at 4 °C. The unbound antibodies were washed with PBST, and the blot was treated with horseradish peroxidase-conjugated secondary antibodies (Cell Signaling Technology) for 1 h at 20 °C. ⁴⁶ Protein was detected using a SuperSignal system (Thermo Fisher Scientific) and a chemiluminescence imaging system (Luminograph I; ATTO, Tokyo, Japan) to visualize protein signals. Immunoblot bands were quantified using ImageJ software (NIH, Bethesda, MD, USA).

Immunofluorescence Microscopy

AGS cells were seeded at 2 × 10⁴ cells/well in a 4-well chamber and incubated for 24 h. The cells were then treated with G.T. 0.5 mg/mL for 24 h followed by Arsenite 100 μM for 1 h. All culture medium was removed and fixed with 4% paraformaldehyde for 10 min, permeabilized with 0.5% Triton X-100 in phosphate-buffered saline (PBS) for 15 min, blocked with 5% goat serum for 1 h and incubated overnight at 4 °C with primary antibodies recognizing G3BP1 (sc-365338, 1:500, Santa Cruz Biotechnology, Dallas, TX, USA). ⁴⁷ Alexa-594 goat antibodies against mouse IgG (1:2000, Thermo Fisher Scientific) were used as secondary antibodies, and nuclei were stained with 4′,6-diamidino-2-phenylindole (DAPI; D1306, Thermo Fisher Scientific). Slides were washed four times with PBS for 10 min each and mounted with ProLong Gold antifade mounting medium (Thermo Fisher Scientific). Images were acquired using a Zeiss LSM 510 Meta confocal laser scanning microscope (Carl Zeiss, Oberkochen, Germany). To assess stress granule (SG) formation, we evaluated G3BP1 as a marker protein. SGs were defined as cytoplasmic G3BP1-positive granules with an area greater than 0.3 μm², and granule formation was quantified.

β-Hexosaminidase Release Assay

RBL-2H3 cells were seeded at a density of 5 × 10⁴ cells/well in 96-well plates and incubated for 24 h. The medium was aspirated, and the cells were washed twice with siraganian buffer (119 mM NaCl, 5 mM KCl, 5.6 mM glucose, 0.4 mM MgCl₂, 25 mM PIPES, 40 mM NaOH, 1 mM CaCl₂, and 0.1% bovine serum albumin; pH 7.2), then incubated in 100 μL siraganian buffer supplemented with compound 48/80 (D073, Sigma) or G.T. for 1 h. ⁴⁸ Compound 48/80 was used as a positive control. The reaction was terminated via incubation at 4 °C for 10 min. The fluorescence intensity of β-hexosaminidase in the supernatant was measured using a β-hexosaminidase activity assay kit (MET-5095, Cell Biolabs, San Diego, CA, USA) by using a 2104 EnVision Multilabel Plate Reader (PerkinElmer, Waltham, MA, USA) at an emission wavelength of 340 nm and an excitation wavelength of 450 nm. The relative fluorescence units of β-hexosaminidase release were calculated by subtracting the fluorescence intensity of the control group from that of the experimental group.

Statistical Analysis

Data are presented as mean ± standard deviation (SD). For the comparison between two groups, data was analyzed using the Student's t-test while for comparison between multiple groups, data was analyzed by one-way analysis of variance (ANOVA) followed by post hoc Tukey HSD. Values of P < .05 were considered significant.

Results

Antioxidant Activity of Grape Tendrils Extracts (G.T)

Fresh grape tendrils were harvested and extracted using 50% ethanol at 50 °C for 6 h (Figure 1A). The TPC of the extract was determined using the Folin-Ciocalteu assay, yielding a concentration of 58.8 ± 1.29 μg GAE/mg extract. The presence of representative polyphenolic compounds, resveratrol and quercetin, was confirmed by HPLC analysis. Using an extract concentration of 100 mg/mL, HPLC revealed that resveratrol was eluted at around 6.4 min with a concentration of 19.6 ng per 1 μg of extract, while quercetin was eluted at approximately 7.2 min with a concentration of 1.45 ng (Figure 1B). Next, the antioxidant activity was evaluated using the ABTS radical scavenging assay. G.T. exhibited dose-dependent antioxidant activity, showing 40% radical scavenging at 1 mg/mL and increasing to 88% at 4 mg/mL. Resveratrol, used as a positive control, demonstrated 40% radical scavenging activity at 25 μg/mL (Figure 1C). These results indicate that G.T. possesses potent antioxidant properties, suggesting its potential role in protecting cellular components from oxidative damage.

Figure 1.

Preparation and antioxidant activity of grape tendril extract (G.T.). (A) Schematic representation of the extraction procedure for grape tendrils from Vitis labruscana Baily × Vitis vinifera Bitis vinifera L. (‘Shine Muscat’) (B) HPLC chromatogram of G.T. extract showing peaks corresponding to resveratrol (Res., 6.38 min) and quercetin (Que., 7.22 min). (C) Radical scavenging activity of resveratrol (Res.) and grape tendril (G.T.) extracts at various concentrations. Resveratrol concentrations are presented in µg/mL, while G.T. concentrations are shown in mg/mL. The corresponding IC₅₀ values are indicated in the figure. Data: mean ± SD (n = 3).

Effects of G.T. on Cell Viability

The cytotoxicity of G.T. was evaluated in multiple cell lines using the MTS assay. Cells were treated with varying concentrations of G.T. (0-2 mg/mL) for 36 h. At concentrations up to 0.5 mg/mL, no significant decrease in cell viability was observed, with AGS and HDF cells showing slightly increased viability. At 1 mg/mL, HaCaT and HDF cells maintained approximately 80% viability, while AGS cells remained unaffected. However, treatment with 2 mg/mL G.T. led to significant decreases in viability across all cell lines (Figure 2). These cytotoxicity profiles establish a safe concentration range for subsequent experiments and demonstrates cell-type specific sensitivity to G.T.

Figure 2.

Cell viability assay of G.T. (0-2 mg/mL, 36 h) in (A) AGS, (B) HaCaT, and (C) HDF cells. Statistical significance was determined using unpaired two-tailed student's t-test. **P < .01, ***P < .001 compared to the untreated control group. Data: mean ± SD (n = 3).

Anti-inflammatory Effects of G.T

The anti-inflammatory activity of G.T. was assessed in RAW 264.7 cells. Cells were pre-treated with G.T. (0.5 or 1 mg/mL) for 24 h followed by LPS (1 μg/mL) stimulation for 6 h. qRT-PCR analysis revealed that G.T. treatment significantly suppressed LPS-induced mRNA expression of pro-inflammatory cytokines TNF-α, IL-6, and IL-1β (Figure 3A). To investigate the underlying mechanism, we examined the NF-κB pathway. Western blot analysis showed that G.T. treatment, particularly at 1 mg/mL, attenuated LPS-induced IκBα phosphorylation after 30 min of LPS stimulation (Figure 3B, Supplementary Figure 1). These findings suggest that G.T. exerts its anti-inflammatory effects primarily through modulation of the NF-κB signaling pathway.

Figure 3.

Anti-inflammatory effects of G.T. in RAW 264.7 cells. (A) Expression of pro-inflammatory cytokines after G.T. (0.5, 1 mg/mL) and LPS (1 μg/mL) treatment. (B) Immunoblot analysis of NF-κB pathway components. M, size marker. Data: mean ± SD (n = 3).

Effect of G.T. on Stress Granule Formation by G.T

The impact of G.T. on stress granule formation was examined in AGS cells under oxidative stress conditions. Cells were pre-treated with 0.5 mg/mL G.T. for 24 h before exposure to arsenite (100 μM) for 1 h. Immunofluorescence microscopy using anti-G3BP1 antibodies revealed that arsenite treatment induced significant stress granule formation (Figure 4A). G.T. pre-treatment significantly reduced both the percentage of SG-positive cells and the number of SGs per cell (Figure 4B and C). In addition, measurement of SG-positive cells revealed that the size of stress granules formed in G.T.-treated cells was significantly reduced by G.T. treatment (Figure 4D). The inhibitory effect of G.T. on stress granule formation correlates with its antioxidant properties, suggesting a potential protective mechanism against oxidative stress-induced cellular damage.

Figure 4.

Effect of G.T. on stress granule formation. (A) Immunofluorescence images of G3BP1 (red) and DAPI (blue) in AGS Cells treated with G.T. (0.5 mg/mL) and arsenite (100 μM). Scale Bar: 20 μm. (B) Percentage of SG-positive cells. (C) Number of SGs per cell. (D) Quantification of stress granule size in cells treated with arsenite (Ars., n = 29) or with both arsenite and G.T. (n = 28). Data: mean ± SD. **P < .01; ***P < .001.

Anti-allergic Activity of G.T

The anti-allergic potential of G.T. was evaluated using RBL-2H3 mast cells. Cells were treated with G.T. (0.5 or 1.0 mg/mL) in the presence of compound 48/80 (1 mg/mL), a known inducer of mast cell degranulation. β-hexosaminidase release assay showed that G.T. significantly inhibited degranulation in a dose-dependent manner. The inhibitory effect was statistically significant at both concentrations tested (P < .05 at 0.5 mg/mL; P < .01 at 1.0 mg/mL) compared to compound 48/80 treatment alone (Figure 5). These results demonstrate that G.T. effectively suppresses mast cell degranulation, indicating its potential therapeutic application in allergic conditions.

Figure 5.

Anti-allergic activity of G.T. β-hexosaminidase release in RBL-2H3 cells treated with G.T. (0.5, 1.0 mg/mL) and compound 48/80 (1 mg/mL). Group comparisons were analyzed using one-way ANOVA with Tukey's HSD test for multiple comparisons. Data: mean ± SD (n = 3). *P < .05, **P < .01, ***P < .001; n.s., not Significant.

Discussion

With the increasing prevalence of chronic diseases and drug resistance, medicinal plants have become a valuable source of bioactive compounds with significant therapeutic potential. Natural products offer promising therapeutic benefits and remain an essential area of research as potential alternatives to synthetic drugs.^49,50

Extensive studies have been conducted on grape-derived antioxidants from various parts of the grapevine, such as seeds, skins, and leaves. These parts are known to exhibit various biological activities, including antioxidant and anti-inflammatory effects.^51-57 In particular, grape seed extract (VGSE) has been reported to exert significant radical-scavenging activity. ⁵⁸ In the present study, G.T. demonstrated comparable biological activity, achieving 88% ABTS radical scavenging activity at 4 mg/mL. These findings suggest that G.T., like other grapevine components, possesses beneficial biological activity and may have superior potential to protect biomolecules from oxidative damage.

These antioxidant properties may be associated with redox-sensitive signaling cascades that interact with anti-inflammatory pathways, particularly the ROS–NF-κB axis. Excessive ROS levels are known to activate NF-κB, thereby promoting the expression of pro-inflammatory genes.^59,60 Thus, the antioxidant capacity of G.T. may indirectly contribute to NF-κB suppression via ROS reduction, as supported by the observed downregulation of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) in this study. Furthermore, G.T. inhibited β-hexosaminidase release in RBL-2H3 mast cells, indicating anti-allergic efficacy. These combined effects provide molecular evidence for the therapeutic potential of G.T. through its antioxidant, anti-inflammatory, and anti-allergic activities. Notably, the newly observed suppression of stress granule formation suggests an additional protective mechanism against cellular stress.

Although these activities were independently observed, further studies are warranted to explore the potential interplay between these biological effects. Moreover, several limitations of this study should be addressed in future research. First, the specific active constituents responsible for G.T.'s effects remain to be identified. Targeted phytochemical profiling and bioactivity-guided fractionation may help identify marker compounds associated with each bioactivity. Second, in vivo studies are needed to validate these findings under physiological conditions. Future studies employing relevant disease models, such as hepatic fibrosis or systemic inflammation models, are needed to confirm the efficacy under physiological conditions. Third, comprehensive toxicological evaluation is required to establish safety profiles for therapeutic applications. Addressing these limitations through future research may support the development of G.T. as a multifunctional natural therapeutic agent.

Conclusion

This study demonstrates significant biological activities of crude grape tendril extract. G.T. exhibited potent antioxidant activity, anti-inflammatory effects through NF-κB pathway inhibition, and anti-allergic properties via mast cell degranulation suppression. Moreover, G.T. showed protective effects against oxidative stress by reducing stress granule formation. Future research should focus on identifying active compounds, evaluating in vivo efficacy, and elucidating detailed mechanisms. These findings establish grape tendril extract as a promising candidate for developing natural therapeutic agents.

Supplemental Material

sj-docx-1-npx-10.1177_1934578X251357816 - Supplemental material for Biological Activities of Crude Grape Tendril Extract Against Oxidative Stress, Inflammation, and Allergy

Supplemental material, sj-docx-1-npx-10.1177_1934578X251357816 for Biological Activities of Crude Grape Tendril Extract Against Oxidative Stress, Inflammation, and Allergy by Si-Eon Kim, Sangsoo Lee, Hui-Je Lee, Da-Min Jung, Jin-Young Lee and Kee K. Kim in Natural Product Communications