Aspidiata E,a New Spirostanol Saponin From Aspidistra triradiata and its Cytotoxic Activity

Abstract

Aspidiata E (1), a new spirostanol saponin {(22S*,25R*)-1β,3β,4β,5β,6β-pentahydroxyspirostan-2β-yl β-D-xylopyranoside), together with 2 known compounds, (22S*,25R*)-spirost-5-ene-3β-yl O-α-L-rhamnopyranosyl-(1→2)-O-[O-α-L-rhamnopyranosyl-(1→5)-α-L-arabinofuranosyl-(1→4)]-β-D-glucopyranoside (2), and (22S*)-16-[(β-D-glucopyranosyl)oxy]-1β,3β,22-trihydroxycholest-5-en-1β-yl α-L-rhamnopyranoside (3), were isolated from Aspidistra triradiata. Their structures were determined by NMR spectroscopic and high resolution electrospray ionisation mass spectrometry analysis and by comparison with published data. Compound 2 revealed strong cytotoxic potential against MCF7, HepG2, SK-LU-1, and HT-29 cancer cell lines with IC₅₀ values ranging from 0.28 to 0.81 µM. In contrast, compound 1 showed a weak inhibitory effect on MCF7, HepG2, and HT-29 cell lines, with IC₅₀ values within the range of 68.85 to 84.19 µM. All compounds 1-3 were discovered for the first time in the genus Aspidistra.

Keywords

Aspidiata E Aspidistra triradiata cytotoxic activity isolation spirostanol saponin

Introduction

The genus Aspidistra Ker Gawler comprises herbaceous rhizomatous plants,¹ which are widely distributed in subtropical and tropical monsoon forests of Southeast Asia, ranging from lowlands up to 1500 m in altitude.² Research into the species diversity of this evergreen genus has long been neglected, since flowers of Aspidistra species are usually located on the ground.² However, in recent decades, many new species have been discovered in southern China and northern Vietnam. As a result, this area is regarded as the center of species diversity of this genus. From 2000 to 2018, the number of Aspidistra species rapidly increased from 55 to more than 170,³ and at least 12 new species were described and reported in 2021. Consequently, the genus Aspidistra currently includes about 200 species, approximately half of which are known to exist in Vietnam.¹

Previous phytochemical studies indicated that saponins are the major constituents of this genus with over 90 compounds being reported.⁴ Fractional extracts as well as isolates from the genus Aspidistra revealed remarkable biological activity including antiviral, antitumor,^5,6 cytotoxic,^4,7 antioxidant,^8,9 and anti-inflammatory effects.¹⁰ In some Asian countries, certain Aspidistra species have been used in traditional medicine for the treatment of fractures, back pain, and hypercholesterolemia.^8,11 Our previous study isolated 5 compounds from A. triradiata, including 1 new spirostanol steroid (aspidiata A) and 1 new spirostanol saponin (aspidiata B), and evaluated the cytotoxicity of these isolates against 4 cancer cell lines.¹² In the ongoing exploration for natural compounds with potential cytotoxic properties from A. triradiata, we have isolated a new spirostanol saponin (1), together with 2 known compounds (2 and 3). Moreover, we report herein the cytotoxic effects of these compounds against 4 human cancer cell lines (SK-LU-1 [lung carcinoma], HepG2 [hepatocarcinoma], MCF7 [breast carcinoma], and HT-29 [colorectal carcinoma]).

Results and Discussion

Compound 1 was obtained as a white, amorphous powder. Its molecular formula was established as C₃₂H₅₂O₁₂ based on the appearance of the sodiated molecular ion at m/z 651.3368 [M + Na]⁺, as well as through the analysis of NMR data. The existence of hydroxy, and ether functional groups in 1 were deduced by IR absorption bands at 3445 and 1061 cm⁻¹, respectively.

The ¹H NMR spectrum of 1 indicated representative signals of 4 methyl groups including 2 singlets at δ_H 0.83 (H₃-18) and 1.87 (H₃-19), and 2 doublets at δ_H 0.66 (H₃-27) and 1.11 (H₃-21) ( Table 1 ). In the HMBC spectrum, H₃-21 and H₂-26 (δ_H 3.47, 3.54) correlated with a spiroacetal carbon at δ_C 109.2 (C-22), whereas the H₃-27 correlated with carbons at δ_C 29.2 (CH₂-24), 30.5 (CH-25), and 66.8 (CH₂-26). These data were indicative of a spirostane-type skeleton.

Table 1.

¹H and ¹³C NMR Data of Compound 1 (in Pyridine-d₅) [δ (ppm), J (Hz)].

Position	^b δ _C	^c δ _H
1	78.7	4.49 brs
2	73.6	4.42 brs
3	72.2	4.97 brs
4	69.6	4.24 brs
5	78.7	-
6	69.4	4.84 brs
7	35.3	1.45^a, 2.05^a
8	30.0	2.35 m
9	45.4	1.27 m
10	45.4	-
11	21.4	1.52^a, 1.58^a
12	39.9	1.06^a, 1.63^a
13	40.6	-
14	55.9	1.11^a
15	32.2	1.42^a, 2.05^a
16	81.0	4.55 m
17	63.0	1.81 t (7.2)
18	16.4	0.83 s
19	15.9	1.87 s
20	42.0	1.92 m
21	15.0	1.11 d (7.2)
22	109.2	-
23	31.8	1.58 d (13.8), 1.65^a
24	29.2	1.52 m
25	30.5	1.55^a
26	66.8	3.47 dd (10.8, 10.2), 3.54 dd (10.8, 3.6)
27	17.2	0.66 d (5.4)
	2-O-Xyl
1′	103.1	5.14 d (7.8)
2′	75.1	4.07 dd (8.4, 7.8)
3′	78.2	4.17 dd (8.4, 8.4)
4′	71.1	4.24^a
5′	67.3	3.74 dd (11.4, 10.2), 4.37 dd (11.4, 6.0)

Assignments were accomplished by ¹H NMR, ¹³C NMR, HSQC, HMBC, COSY, and ROESY experiments.

Xyl, β-D-xylopyranosyl.

aOverlapping signals.

b150 MHz.

c600 MHz.

Additionally, the attendance of 1 sugar unit was deduced by a signal for 1 anomeric proton at δ_H 5.14 (1H, d, J = 7.8 Hz) correlating with an anomeric carbon at δ_C 103.1. The ¹³C NMR spectrum of 1 combined with HSQC experiment showed 32 signals, including 14 oxygenated sp³ carbons (δ_C 66.8, 67.3, 69.4, 69.6, 71.1, 72.2, 73.6, 75.1, 78.2, 78.7, 78.7, 81.0, 103.1, and 109.2). Thus, compound 1 was proposed as a polyoxygenated spirostanol saponin ( Figure 1 ).

Figure 1.

Chemical structures of compounds 1-3.

The ¹H and ¹³C NMR spectroscopic data of 1 were similar to those of (25R)-spirostan-1β,2β,3β,4β,5β,6β-hexol,¹³ except for the addition of 1 sugar unit. The planar structure of the aglycone of 1 was deduced as spirostan-1,2,3,4,5,6-hexol based on the HMBC and COSY experiments ( Figure 2 ). The compounds relative configuration was established by ROESY data together with coupling constant (J) analysis. Particularly, H-2 (δ_H 4.42)/H-4 showed ROESY correlations with H-9 (δ_H 1.27) ( Figure 3 ). This evidence confirmed the cis-fused ring junction between the A and B rings, as well as the α-axial (ax) orientations of H-2 and H-4 in the A ring's chair-shaped conformation. The α-equatorial (eq) orientation was attributed for H-1 based on the ROESY correlation between H-1 and H-9. This is also supported by the small J value between the H-1 α-eq and the H-2 α-ax. The broad singlet signal of H-3 (δ_H 4.97), which was attributed to a small J value, indicated an eq-ax relationship with H _α -2 (δ_H 4.42)/H _α -4 (δ_H 4.24), hence concluding the α-equatorial orientation of H-3. Similarly, H-6 is located in the α-eq orientation of the B ring because this proton appeared as a broad singlet which associated with eq-ax and eq-eq relations between H-6 and H₂-7 (δ_H 1.45, 2.05). This conclusion was strengthened by the ROESY cross peak of H-6 to H _α -4.

Figure 2.

Key HMBC (¹H→¹³C, arrows) and COSY (bold lines, different colors) correlations of 1.

Figure 3.

Key ROESY correlations (dashed arrows) of 1.

The ROESY correlations of H-20 (δ_H 1.92)/H₃-18, H-16 (δ_H 4.55)/H₃-21 implied that the CH₃-21 and H-20 groups were oriented in α and β, respectively. Because H-20 resonated at higher field than δ_H 2.2, the orientation relationships between this proton and the oxygen atom on F ring was trans.¹⁴ Consequently, the S* configuration was assigned for C-22.¹⁵ The ¹³C NMR data of the F ring and C-27 [δ_C 109.2 (C-22), 31.8 (C-23), 29.2 (C-24), 30.5 (C-25), 66.8 (C-26), 17.2 (C-27)] of 1 totally agreed with those of (25R)-5β-spirostan-3β-ol-12-one-3-O-β-D-glucopyranoside [δ_C 109.3 (C-22), 31.8 (C-23), 29.2 (C-24), 30.5 (C-25), 66.9 (C-26), 17.3 (C-27)], and differed from those of the (25S)-stereoisomer [δ_C 109.8 (C-22), 26.4 (C-23), 26.1 (C-24), 27.5 (C-25), 65.2 (C-26), 16.3 (C-27)].^4,16 Moreover, the small difference in δ_H values of the 2 protons at C-26 (Δ_ea = δ_H-26eq−δ_H-26ax = 0.07) of 1 agreed with that of the (25R) form (25R: Δ_ea < 0.20; 25S: Δ_ea > 0.35).¹⁷ Therefore, the R* configuration was suggested for C-25 of 1. This was further confirmed by the ROESY correlations of H₃-27 to H₂-24 (δ_H 1.52)/H-26. All of the above analyses have determined the aglycone of 1 to be (22S*,25R*)-spirostan-1β,2β,3β,4β,5β,6β-hexol.

A series of reactions, including hydrolysis of 1, reduction, per-acetylated derivatization, and then GC-MS analysis, was performed to elucidate the monosaccharide composition of 1. As a result, D-xylose was determined as the only sugar unit of 1. By consideration of 1D- and 2D-NMR spectra and the J value of the anomeric position, this carbohydrate moiety was further confirmed to be β-D-xylopyranose. In particular, the HMBC correlation of the oxymethylene protons H₂-5ʹ (δ_H 3.74, 4.37) to the anomeric carbon (δ_C 103.1) proved the pyran form of xylose. In addition, the anomeric coupling constant value of 7.8 Hz indicated the β-configuration of this sugar. The strong correlation observed in the HMBC spectrum between H-1ʹ (δ_H 5.14, d, J = 7.8 Hz) and C-2 (δ_C 73.6), coupled with the ROESY correlation of H-1ʹ to H-2 confirmed that the β-D-xylopyranosyl moiety was linked to C-2 of the aglycone. Consequently, the complete structure of 1 was elucidated as (22S*,25R*)-1β,3β,4β,5β,6β-pentahydroxyspirostan-2β-yl β-D-xylopyranoside, and named aspidiata E (Supplemental Figures S1 – S14).

The remaining compounds were confirmed as (22S*,25R*)-spirost-5-ene-3β-yl O-α-L-rhamnopyranosyl-(1→2)-O-[O-α-L-rhamnopyranosyl-(1→5)-α-L-arabinofuranosyl-(1→4)]-β-D-glucopyranoside (2),¹⁸ and (22S*)-16-[(β-D-glucopyranosyl)oxy]-1β,3β,22-trihydroxycholest-5-en-1β-yl α-L-rhamnopyranoside (3)¹⁹ by comparisons of their NMR data with literature values (Supplemental Table S1 and Supplemental Figures S15 – S37). This is the first report on the isolation of 1-3 from the genus Aspidistra.

The sulforhodamine B (SRB) assay was used to access the cytotoxic potential of the isolated compounds against MCF-7, SK-LU-1, HepG2, and HT-29 human cancer cell lines ( Table 2 ). Compound 2 displayed a potent cytotoxic effect on the evaluated cell lines, with IC₅₀ values ranging from 0.28 ± 0.02 to 0.81 ± 0.07 µM. Notably, the activity of 2 was even more significant than that of the positive control on the 4 cell lines. Compound 1 exhibited a weak inhibitory effect on MCF7, HepG2, and HT-29 cell lines, with IC₅₀ values ranging from 68.85 ± 5.36 to 84.19 ± 5.61 µM. In contrast, compound 3 did not show any cytotoxicity. Mimaki et al reported that the cholestane glycoside 3 showed no activity against the HL-60 (human promyelocytic leukemia) cell line.²⁰ Meanwhile, the spirostanol saponin 2 revealed significant cytotoxicity against HL-60 cells, with an IC₅₀ value of 0.52 µg/mL.²¹

Table 2.

Cytotoxicities of 1-3 Against Human Cancer Cell Lines.

Cell lines	IC₅₀ ^a (µM)
Cell lines	MCF7	HepG2	SK-LU-1	HT-29
1	83.30 ± 3.59	68.85 ± 5.36	>100	84.19 ± 5.61
2	0.36 ± 0.05	0.81 ± 0.07	0.57 ± 0.02	0.28 ± 0.02
3	>100	>100	>100	>100
Ellipticine ^b	1.54 ± 0.08	1.34 ± 0.16	1.87 ± 0.16	1.34 ± 0.08

aIC₅₀ (concentration that inhibits 50% of cell growth).

bPositive control.

Based on our results, the following cytotoxic structure-activity relationships can be revealed. Regarding the spirostanol saponins without a hydroxyl group at C-17, such as compounds 1 and 2, the cytotoxic effects depend on the presence/absence of a double bond at C-5 and C-6, and the hydroxyl groups of the aglycone part. Compounds with double bonds at C-5, C-6 and no hydroxyl group in the aglycone part, such as compound 2, gracillin, diosgenin-3-O-α-L-arabinofuranosyl-(1→4)-β-D-glucopyranoside, prosapogenin A of dioscin, reclinatoside, loureiroside,²¹ dioscin,²² progenin II,²² and progenin III²² exhibit significant cytotoxic effects. Meanwhile, compounds that do not possess double bonds at C-5 or C-6 but possess hydroxyl group(s) in the aglycone part, such as compound 1 and parisvientnaside A,²¹ show weak cytotoxic activity. For cholestane glycosides, a study by Kuroda et al.²³ revealed that the presence of a carbonyl group at C-22 instead of a hydroxyl group increased the cytotoxic effect. Consequently, compound 2 should be assessed for its cytotoxicity against other cancer cell lines, and for its cytotoxic mechanisms.

Conclusion

Through an investigation of the chemical composition of A. triradiata, a new spirostanol saponin, aspidiata E (1), was isolated together with 2 known compounds, (22S*,25R*)-spirost-5-ene-3β-yl O-α-L-rhamnopyranosyl-(1→2)-O-[O-α-L-rhamnopyranosyl-(1→5)-α-L-arabinofuranosyl-(1→4)]-β-D-glucopyranoside (2), and (22S*)-16-[(β-D-glucopyranosyl)oxy]-1β,3β,22-trihydroxycholest-5-en-1β-yl α-L-rhamnopyranoside (3). Compound 2 showed very good cytotoxic activity against MCF7, HepG2, SK-LU-1, and HT-29 cell lines with IC₅₀ values in the range of 0.28 to 0.81 µM, while compound 1 exhibited a weak inhibitory effect on MCF7, HepG2, and HT-29 cell lines, as illustrated by IC₅₀ values in the range of 68.85 to 84.19 µM. The results indicated a therapeutically significant cytotoxic effect of compound 2, suggesting that this compound could show potential in further investigations of anticancer mechanisms.

Materials and Methods

General Experimental Procedures

Optical rotations were recorded on a JASCO-2000 Polarimeter (JASCO, Tokyo, Japan), IR spectra on an IR Prestige-21 spectrometer (Shimadzu, Kyoto, Japan), NMR spectra on Bruker Avance Neo 600 (Bruker, Billerica, MA, USA) and Bruker Avance 500 spectrometers (Bruker, Billerica, MA, USA), and high resolution electrospray ionisation mass spectrometry (HRESIMS) on an Agilent 6530 Accurate-Mass spectrometer (Agilent, Santa Monica, CA, USA). Normal-phase silica gel (40-50 µm, Kanto Chemical, Tokyo, Japan), C18 reverse-phase silica gel (Fuji Silysia Chemical, Aichi, Japan), and Sephadex LH-20 (Sigma-Aldrich, St. Louis, MO, USA) were employed for column chromatography. Analytical thin-layer chromatography was conducted using pre-coated silica gel 60 F₂₅₄ and silica gel 60 RP-18 F₂₅₄ plates (Merck, Darmstadt, Germany). The cancer cell lines were acquired from Long Island University (Brooklyn and Brookville, NY, USA). The 96-well plates were procured from Corning (Corning, NY, USA). The cytotoxic activity assay concluded with the measurement of cell absorbance using an ELISA Plate Reader (Agilent BioTek, Santa Monica, CA, USA).

Plant Material

In March 2020, whole A. triradiata plants were collected from Quang Tri province, Vietnam (16° 29′ 20.6"N 107° 00′ 33.1"E) and authenticated by Dr Nguyen The Cuong of the Institute of Ecology and Biological Resources, VAST, Vietnam. To serve as a reference, a specimen labeled AT-01 is preserved at the Faculty of Pharmacy, Hue University of Medicine and Pharmacy, Hue University, Vietnam.

Extraction and Isolation

The entire dried plant of A. triradiata (3.31 kg) was ground into powder and subjected to maceration with MeOH at room temperature. After the solvent was eliminated under vacuum, a MeOH extract weighing 550 g was acquired. This extract was then dispersed in water and fractionated continuously using hexane, ethyl acetate (EtOAc), and 1-butanol (BuOH) (3 times, each 4.0 L) to give the respective fractions.

The BuOH fraction (201.2 g) was separated on a normal phase open column by elution with CH₂Cl₂-MeOH-H₂O (6:1:0.1, v/v) to gain 13 fractions, B1-B13. Fraction B9 (4.6 g) was subjected to partitioning on a YMC RP-18 column, using Me₂CO-MeOH-H₂O (1.5:1:1, v/v) as an eluent, resulting in 5 fractions, B9.1-B9.5. Fraction B9.4 (783.0 mg) was chromatographed on a silica gel column and eluted with CH₂Cl₂-MeOH-TFA 0.1%/H₂O (5.5:1:0.1, v/v) to give 4 fractions, B9.4.1-B9.4.4. Fraction B9.4.2 (278.4 mg) was further purified by RP-18 column chromatography and elution with Me₂CO-MeOH-H₂O (2.7:1:1, v/v) to afford 2 (39.0 mg). Using MeOH-H₂O (5:1, v/v) as the eluent, fraction B10 (30.7 g) was separated into 6 sub-fractions, B10.1-B10.6, through fractionation on a RP-18 column. Further purification of fraction B10.3 (937.0 mg) was carried out by Sephadex LH-20 column chromatography, and elution with MeOH-H₂O (3:1, v/v) to obtain 3 fractions, B10.3.1-B10.3.3. Compound 1 (11.0 mg) was obtained from fraction B10.3.3 (65.3 mg) by separation on a YMC RP-18 column by elution with Me₂CO-MeOH-H₂O (0.5:2:1, v/v).

The EtOAc fraction (92.0 g) was passed through a silica gel column using a stepwise gradient mixture of hexane-EtOAc (100:0-0:100, v/v) to give 7 fractions, E1-E7. Further chromatography of fraction E6 (16.4 g) on a silica gel column with the eluent CH₂Cl₂-EtOAc-MeOH (10:2:1, v/v) resulted in 12 fractions, E6.1-E6.12. By subjecting fraction E6.12 (119.5 mg) to chromatography on a RP-18 column with the eluent MeOH-H₂O (3.5:1, v/v), 4 fractions, E6.12.1-E6.12.4 were yielded. Lastly, fraction E6.12.1 (42.0 mg) was fractionated by Sephadex LH-20 column chromatography and elution with MeOH-H₂O (4:1, v/v) to furnish 3 (19.0 mg).

Aspidiata E (1) White amorphous powder; [a]_D²⁷ + 222.8 (c 0.1 MeOH); IR (KBr) ν_max (cm⁻¹): 3445, 2943, 2851, 1638, 1452, 1402, 1244, 1157, 1060, 982, 926, 901, 868, 675, 517; HRESIMS m/z 651.3368 [M + Na]⁺ (calcd. for C₃₂H₅₂O₁₂Na⁺, 651.3351); ¹H NMR (600 MHz, pyridine-d₅), ¹³C NMR (150 MHz, pyridine-d₅): see Table 1 .

Determination of the Monosaccharide Composition of 1

The method of Pettolino et al.²⁴ with minor alterations was used to clarify the monosaccharide constituent of compound 1. The methodology was carried out following the procedure outlined in our previous publication.⁴

SRB Assay for Determining Cytotoxic Activity

The SRB assay²⁵ was carried out to evaluate the cytotoxicity of the isolated compounds on 4 cancer cell lines. The cells were grown in Dulbecco's modified Eagle medium consisting of 1.5 g/L sodium bicarbonate, 2 mM L-glutamine, and 10% fetal bovine serum, with a media change every 48 h. The cells were separated by 0.05% (w/v) trypsin-EDTA, further cultured at a scale of 1:3 every 3 to 5 days, and maintained under a 5% CO₂/atmosphere at 37 °C. After 48 h of incubation, the viable cells were seeded into 96-well plates at a density of 4 × 10⁴ cells/well in growth medium (180 µL) and allowed to attach for 12 h. The cells were then treated with varying concentrations of test samples and incubated in the same state for 72 h. After eliminating the medium, cold 20% (w/v) trichloroacetic acid was supplemented to stabilize the remaining cells for 1 h at 4 °C. The cells were stained by adding 1X SRB solution and maintained for 30 min. The disconnected dye was eliminated by continual washing with 1% (v/v) acetic acid, while the dye bound to the cellular proteins was dissolved in 10 mM Tris base. The optical density was measured using an ELISA Plate Reader at a wavelength of 515 nm. The positive reference control was ellipticine, while 10% dimethyl sulfoxide served as the blank sample. The TableCurve 2Dv4 program was used to calculate the concentration giving 50% inhibition (IC₅₀) to illustrate cytotoxic activity. Data were the average of 3 independent experiments. The cell inhibition rates (IR) were calculated by the following formula, in which OD₀ and OD_t represent the mean optical density values at time zero and day 3, respectively, while OD_c represents the mean optical density value of the blank:

I R % = 100 % – [(O D_{t} – O D_{0}) / (O D_{c} – O D_{0})] \times 100.

Supplemental Material

sj-docx-1-npx-10.1177_1934578X231179412 - Supplemental material for Aspidiata E, a New Spirostanol Saponin From Aspidistra triradiata and its Cytotoxic Activity

Supplemental material, sj-docx-1-npx-10.1177_1934578X231179412 for Aspidiata E, a New Spirostanol Saponin From Aspidistra triradiata and its Cytotoxic Activity by Hien Bich Thi Le, Van Anh Thi Tran, Hien Minh Nguyen and Linh Thuy Khanh Nguyen, Duc Viet Ho, Hoai Thi Nguyen in Natural Product Communications

Footnotes

Acknowledgments

We are grateful to Mr Luong Vu Dang (Institute of Chemistry, VAST, Hanoi, Vietnam) for recording the NMR spectra.

Declaration of Conflicting Interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Ethical Approval

Not applicable, because this article does not contain any studies with human or animal subjects.

Funding

The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was financially supported by Hue University under Grant (ID No. DHH2022-04-160). Le Thi Bich Hien was funded by the Master, PhD Scholarship Programme of Vingroup Innovation Foundation (VINIF), code VINIF.2022.TS039. The authors also acknowledge the partial support of Hue University under the Core Research Program, Grant No. NCM.DHH.2023.02.

Informed Consent

Not applicable, because this article does not contain any studies with human or animal subjects.

ORCID iDs

Duc Viet Ho

Hien Minh Nguyen

Hoai Thi Nguyen

Trial Registration

Not applicable, because this article does not contain any clinical trials.

Supplemental Material

Supplemental material for this article is available online.

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