Platycladus orientalis (L.) Franco demonstrates effective anti-psoriasis effects by inhibiting PDE4 with favorable safety profiles
Qing Zhang , Ling Sun , Lingyu Wu , Xue Wang , Liru Chen , Youyou Chen , Yuhang Liu , Wenhui Gu , Donglei Shi , Wenwen Liu , Jian Li , Yi-You Huang , Baoli Li , Hai-Bin Luo
Psoriasis is a chronic inflammatory skin disorder, characterized by erythematous plaques covered with silvery-white scales, often accompanied by symptoms such as itching, burning, dryness, cracking, and in severe cases, bleeding. Currently, the incidence of psoriasis exhibits an escalating trajectory [1]. Epidemiological surveys indicate an approximate prevalence rate of 0.47% in China, affecting over 7 million people, thereby imposing a substantial societal burden [2]. Current treatments for psoriasis include biologics and pharmacotherapies. Biologics predominantly consist of tumor necrosis factor-α (TNF-α) antagonists [3], interleukin 17 (IL-17) antibodies [4,5], and IL-23 antibodies [6,7]. However, existing biologics precipitate grave adverse reactions, and most require parenteral administration, leading to considerable discomfort for patients [8,9]. Non-biologic treatments, such as calcipotriol, a vitamin D3 derivative, are effective in mitigating psoriasis by impeding keratinocyte proliferation and promoting keratinocyte apoptosis [10]. However, its long-term or widespread use is limited, as exceeding a weekly dosage of 100 g may result in hypercalcemia.
Phosphodiesterase-4 (PDE4) is a key enzyme responsible for the breakdown of cyclic adenosine monophosphate (cAMP) [11,12]. Studies have shown that PDE4B and PDE4D mRNA are overexpressed in peripheral blood mononuclear cells (PBMC) of patients with psoriasis [13]. By modulating the concentration of cAMP, PDE4 initiates downstream phosphorylation cascades to regulate the network of pro-inflammatory and anti-inflammatory mediators, making it an effective target for psoriasis treatment [14-16]. Apremilast, a PDE4 inhibitor, was the first oral therapy approved in adult patients with plaque psoriasis of all disease severity levels, including mild, moderate, and severe. It was approved by the US Food and Drug Administration (FDA) and the European Medicines Agency (EMA) in 2014 for the treatment of psoriasis and psoriatic arthritis, and achieved global sales of $2.188 billion in 2023. By increasing the concentration of intracellular cAMP, apremilast promotes the production of anti-inflammatory mediators while reducing the production of pro-inflammatory factors, thereby regulating the inflammatory response in psoriasis. Specifically, increased cAMP concentration activates cAMP-dependent protein kinase A (PKA), which in turn activates transcription factors such as cAMP reaction original binding protein (CREB), promotes the production of anti-inflammatory mediators such as IL-10, and reduces the production of pro-inflammatory factors such as IL-23, TNF-α, and interferon γ (IFN-γ). In vitro, PDE4 inhibitors are able to reduce PBMC production of many pro-inflammatory cytokines and increase levels of anti-inflammatory mediators. In vivo, PDE4 inhibitors exert therapeutic effects on psoriasis by regulating cAMP levels and affecting IL-23 secretion. However, clinical studies of existing PDE4 inhibitors have revealed a high incidence of gastrointestinal adverse effects, such as nausea and vomiting, which limit their clinical utility [13]. Given these challenges, the pursuit of safer and more reliable PDE4 inhibitors remains a critical priority.
Natural products have emerged as a vital source for the discovery of new therapeutic agents due to their safety profiles and minimal side effects. This highlights the potential of natural products as a source of effective and safer PDE4 inhibitors for psoriasis treatment. Recently, a PDE4 inhibitor screening campaign was conducted using our in-house library of 1200 methanolic extracts from Chinese medicinal plants by protocols similar to our previous reports (Fig. 1A, Sections S1 and S2 in Supporting information) [17-19]. Among these, the methanolic extract of Platycladus orientalis (L.) Franco (P. orientalis) demonstrated notable PDE4 inhibitory activity, achieving 42.7% at a concentration of as low as 0.2 µg/mL (Fig. 1A and Table 1). P. orientalis, commonly known as Chinese arborvitae, is recognized in China as both a medicinal and edible species, highlighting its long-standing history of use. As a traditional herb widely used in Chinese medicine, it is renowned for its therapeutic properties, further reinforcing the potential safety and efficacy in treating psoriasis.
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| Extract/compound | PDE4D inhibitory rate (%) | IC50 (µmol/L) | |
| 1 µg/mL | 0.2 µg/mL | ||
| P. orientalis-MeOH | 90.7 | 42.7 | n.s.b |
| P. orientalis-PE | 89.3 | 26.9 | n.s.b |
| P. orientalis-EA | 95.0 | 56.4 | n.s.b |
| P. orientalis-BtOH | 35.4 | 11.6 | n.s.b |
| P. orientalis-H2O | 17.0 | 1.9 | n.s.b |
| Myricitrin (1) | 6.5 | 1.8 | 40.0 ± 1.1 |
| Quercitrin (2) | 0.4 | 1.7 | 10.0 ± 0.7 |
| Afzelin (3) | 15.4 | 7.8 | 35.8 ± 0.4 |
| AMF (4) | 102.5 | 89.7 | 0.012 ± 0.001 |
| Hinokiflavone (5) | 79.1 | 13.5 | 0.773 ± 0.102 |
| FLDs | 105.4 | 74.2 | n.s.b |
| Roliprama | 56.2a | n.s.b | 0.590 ± 0.050 |
| a Positive control, at a concentration of 800 nmol/L. b Activity was not tested. |
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To further investigate the inhibitory activity of extracts from different polarity fractions on PDE4, the methanolic extract of P. orientalis (P. orientalis-MeOH) was suspended in H2O and successively partitioned with petroleum ether (PE), ethyl acetate (EA), and n-butanol (BtOH), which resulted the following fractions: P. orientalis-PE, P. orientalis-EA, P. orientalis-BtOH, and residual P. orientalis-H2O, respectively. Among these, P. orientalis-EA exhibited the most potent activity with 56.4% inhibition at 0.2 µg/mL (Table 1). High performance liquid chromatograph (HPLC) analysis of P. orientalis-EA at 254 nm revealed five major peaks (Fig. 1B). Further purification by column chromatography (Section S3 in Supporting information) led to the isolation of five compounds: myricitrin (1), quercitrin (2), afzelin (3), amentoflavone (AMF) (4), and hinokiflavone (5) (Fig. 1C). Their structural identities were confirmed through comparative analyses of proton nuclear magnetic resonance (1H NMR) spectroscopy and high-resolution mass spectrometry (HRMS) data (Section S4 in Supporting information) against literature values [20-25].
The inhibitory potencies of compounds 1–5 against PDE4D were also individually investigated, with AMF (4) demonstrating the strongest inhibitory activity, achieving a half maximal inhibitory concentration (IC50) of 0.012 µmol/L. The other four compounds also displayed varying degrees of inhibitory activity (Table 1). Additionally, as shown in Figs. 2A–C, the microscale thermophoresis (MST) method was used to test the binding affinities of compounds 2, 4 and 5 with Kd values of 6.38 mmol/L, 7.42 µmol/L and 127 µmol/L, respectively, which were consistent with the enzymatic activity. Referring to the crystal structure of PDE4D with AMF (4) (Fig. 2D, PDB: pdb:8YLC) [25], the binding patterns of compounds 2 and 5 were also explored by docking method CDOCKER implemented in Discovery Studio with default parameters. As depicted in Figs. 2E and F, compounds 5 and 2 could form H-bonds with Q369 and stacking interactions with the hydrophobic clamp consisting of residues F372, I336, and F340 in the catalytic pocket. These interactions contributed to the fundamental binding of these compounds and were characteristic of all PDE inhibitors. The catechol moiety of compound 2 could aptly make two H-bonds with Q369, nevertheless, 1 and 3 with one more or less hydroxyl group exhibited decreased PDE4D activities. Furthermore, one of the flavonoid fragments in compound 5 could yield a direct or water-mediated H-bond network with residues N321 and T333, but the other flavonoid fragment barely made contacts with PDE4D, which might lead to its relatively lower potency compared with AMF (4).
AMF, a well-known biflavonoid, has been reported to possess various biological activities, such as anti-inflammatory, anti-tumor, hypoglycemic, and neuroprotective properties [23]. Recently, we isolated AMF from another Chinese medicinal plant Selaginella uncinata and established that AMF is a potent PDE4 inhibitor, showing remarkable anti-fibrotic effects [25]. However, the content of AMF in crude extracts from plants, including both P. orientalis and Selaginella uncinate, is relatively low (6.2%), making the acquisition of large quantities of pure AMF challenging. This limitation could significantly hinder its industrial development and medical applications.
To address this challenge and enrich the flavonoid and AMF content from P. orientalis, we developed a purification protocol using macroporous resin. Briefly, the methanolic crude extract was adsorbed onto a macroporous resin column and eluted sequentially with water and ethanol solutions of increasing concentration (Fig. 1A, Section S5 in Supporting information). This method effectively concentrated the AMF content from 6.2% to 72.3%, and the resulting enriched extract was termed flavonoid-rich extract (FLDs) (Fig. 1B). Notably, FLDs exhibited PDE4 inhibitory activity comparable to that of pure AMF (Table 1). This suggests that the prepared FLDs and purified AMF may offer similar therapeutic potential for the treatment of PDE4-related inflammatory diseases, such as psoriasis. The in vitro anti-psoriatic effects of compound AMF and FLDs were firstly evaluated in M5-induced HaCaT cell model stimulating the over-proliferation and inflammation processes of psoriasis as described in prior studies (Fig. 3A) [26]. The anti-proliferation activities of AMF and FLDs were tested at different concentration gradients. As a result, both AMF and FLDs at 100 µg/mL could effectively inhibit abnormal cell proliferation and significantly reduce the expression levels of several inflammatory cytokines, including IL-1α, IL-1β, IL-6, and IL-8, as shown in Figs. 3B and C. These results indicated the potential of AMF and FLDs in alleviating the excessive proliferation and inflammation characteristics of psoriasis, highlighting their therapeutic promise. To some extent, the FLDs seemed to be more effective to inhibit the expression of inflammatory cytokines than AMF.
Besides, the in vivo anti-psoriatic effects of AMF and FLDs were assessed in the imiquimod (IMQ) induced psoriasis-like mouse model (Fig. 4A). All animal care and experimental programs were in line with the "Guide of Laboratory Animals" (National Institutes of Health Publication, revised 1996, No. 86–23, Bethesda, MD) and approved by the Institutional Ethical Committee for Animal Research of Hainan University (No. HPIACUC2024026). In the IMQ group, mice displayed significant skin thickening and erythema, with progressively increasing psoriasis area and severity index (PASI) scores (Fig. 4B), which demonstrated the successful establishment of psoriasis model. Oral administration (p.o.) of AMF at a dosage of 20 mg/kg once daily (qd) demonstrated superior potency compared to Apremilast (20 mg/kg, p.o., qd), as evidenced by reduced severity of skin erythema, scaling, skin thickness, and PASI (Figs. 4B–F). Ointments containing 10% and 20% FLDs were formulated using an emulsification method (Section S6 in Supporting information). The 10% FLDs was topically administrated (t.a.) either qd or twice daily (bid), while the 20% FLDs was topically administrated qd. Notably, all FLDs treatment groups, particularly the 10% bid group, exhibited more pronounced therapeutic effects compared to AMF and apremilast, nearly reversing the thickening, scaling, erythema, and PASI by day 5 (Figs. 4B–F). This suggests a synergistic potency of the five flavonoids against PDE4. Moreover, FLDs mitigated IMQ-induced weight loss in mice and the 10% bid group still exhibited the most potential (Fig. 4G). Additionally, FLDs elevated cAMP levels and reduced inflammatory factors TNF-α, IL-6, IL-17A and IL-23 (Figs. 5A–E). Histopathological analysis, using hematoxylin and eosin (HE) staining, the IMQ model group exhibited significant keratinocyte proliferation in the epidermis, along with characteristic psoriatic features such as hyperkeratosis, parakeratosis, and elongated rete ridges extending into the dermis. Following treatments with FLDs, a marked reduction in keratinocyte proliferation was observed, resulting in a thinner stratum corneum compared to the IMQ group, which corresponded with a reduction in scaling (Figs. 5F and G). Moreover, the infiltration of mononuclear leukocytes in the dermis was significantly reduced, indicating that FLDs effectively suppressed inflammation in psoriatic skin (Fig. 5F). Immunohistochemical analysis further supported these findings. The expression of CD3+ T cells (Figs. 5H and I) and TNF-α (Figs. 5J and K), both key markers of inflammation and immune response in psoriasis, were substantially decreased in the FLDs-treated groups compared to the IMQ group. These results collectively demonstrated that FLDs significantly ameliorate the pathological features of psoriasis, highlighting their therapeutic potential in managing this chronic inflammatory condition.
To further assess the potential of FLDs as a candidate drug for psoriasis, we conducted a comprehensive evaluation of its local irritancy and subacute toxicity in mice and New Zealand rabbits. All animal care and experimental programs were in line with the "Guide of Laboratory Animals" (National Institutes of Health Publication, revised 1996, No. 86–23, Bethesda, MD) and approved by the Institutional Ethical Committee for Animal Research of Hainan University (Nos. HPIACUC2024046 and HPIACUC2024099). A high-dose 30% FLDs ointment was applied to the dorsal skin of normal mice once daily for one week. An IMQ control group was included for comparison without any treatment, and subsequent monitoring was conducted for any pathological changes. The mice exhibited no signs of skin irritation on the dorsal area, and there were no effects on body weight or any changes observed in major organs such as the heart, liver, spleen, or kidneys (Figs. 6A and B). Additionally, there were no symptoms of erythema, edema, or other irritant responses (Section S7 in Supporting information).
Subsequently, we extended the evaluation to New Zealand rabbits, whose skin closely resembles that of humans. To better simulate clinical conditions of psoriasis, we induced skin abrasions and minor bleeding using sandpaper prior to applying FLDs, along with normal group as control. Over a two-week administration period, followed by a recovery phase, rabbits were treated with 30% FLDs ointment at dosages of 2 or 5 g once daily on abraded skin, as well as 5 g once daily on normal skin. The treated rabbits exhibited no significant differences in epidermal condition in abraded skin groups or normal skin group (Figs. 6C and D). Histological examination via HE staining revealed no pathological changes in major organs, indicating an absence of systemic toxicity (Fig. 6E). Furthermore, other physiological parameters, such as body temperature, food intake, and fecal characteristics, remained consistent with the control groups. Hematological analysis, including red and white blood cell counts and hemoglobin levels, showed no significant differences (Section S9 in Supporting information). Blood biochemical analysis confirmed that key metabolic parameters, such as glucose metabolism, lipid metabolism, liver function, and renal function, remained within normal limits in the treated rabbits, further affirming the safety profiles. These comprehensive evaluations demonstrated that FLDs are non-irritating, safe, and nontoxic when applied to both abraded and normal skin in rabbits. Taken together, the toxicity studies in mice and New Zealand rabbits confirm that FLDs is a safe and promising candidate for the treatment of psoriasis.
In this study, we identified FLDs, purified via macroporous resin from P. orientalis, as potent inhibitors of PDE4 that effectively alleviated IMQ-induced psoriasis symptoms in mice, reversing pathological skin changes and reducing inflammatory cytokine levels. Moreover, subacute toxicity studies in mice and rabbits confirmed the safety of FLDs, showing no adverse effects on skin, organs, or blood biochemistry parameters.
These findings establish FLDs from P. orientalis as a promising new therapeutic candidate for psoriasis, offering a novel mechanism of action through PDE4 inhibition. This discovery not only adds a valuable new option to the existing arsenal of psoriasis treatments but also paves the way for further clinical development. Future studies will focus on optimizing the formulation and evaluating the clinical efficacy of FLDs in human trials, with the aim of providing a safer, more effective, and long-time treatment option for psoriasis patients.
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Qing Zhang: Writing – original draft, Methodology, Investigation, Data curation. Ling Sun: Writing – original draft, Validation, Methodology. Lingyu Wu: Writing – original draft, Validation, Investigation, Data curation. Xue Wang: Validation, Methodology. Liru Chen: Investigation, Formal analysis, Data curation. Youyou Chen: Formal analysis, Data curation. Yuhang Liu: Formal analysis, Data curation, Conceptualization. Wenhui Gu: Software, Resources, Data curation. Donglei Shi: Writing – original draft, Validation, Methodology. Wenwen Liu: Methodology, Formal analysis. Jian Li: Writing – review & editing, Resources. Yi-You Huang: Writing – original draft, Validation, Methodology, Conceptualization. Baoli Li: Writing – review & editing, Writing – original draft, Validation, Software, Resources, Project administration, Methodology, Investigation, Conceptualization. Hai-Bin Luo: Writing – review & editing, Writing – original draft, Visualization, Validation, Supervision, Funding acquisition.
This work was supported by the National Key R & D Program of China (No. 2023YFF1205102), National Natural Science Foundation of China (Nos. 22277019, 22307031, 22377023 and 22077143), the Fundamental Research Funds for Hainan University (Nos. RZ2200001094, KYQD(ZR)−21031, and KYQD(ZR)−21108), Collaborative Innovation Center Funds for Hainan University (No. XTCX2022JKA01), and the Science Foundation of Hainan Province (Nos. KJRC2023B10 and 824YXQN420).
Supplementary material associated with this article can be found, in the online version, at doi:
M.A. Lowes, A.M. Bowcock, J.G. Krueger, Nature 445 (2007) 866–873. doi: 10.1038/nature05663
X.J. Zhang, Chin. J. Dermatol. 56 (2023) 573–625. doi: 10.3390/fractalfract7080573
Y. Duan, W. Sun, Y. Li, et al., Acta Pharm. Sin. B 14 (2024) 2646–2656. doi: 10.1016/j.apsb.2024.02.002
R. Oliver, J. Krueger, S. Glatt, et al., Br. J. Dermatol. 186 (2022) 652–663. doi: 10.1111/bjd.20827
S.Y. Paek, J. Frieder, D. Kivelevitch, et al., Semin. Cutaneous Med. Surg. 37 (2018) 148–157. doi: 10.12788/j.sder.2018.051
A. Vu, C. Ulschmid, K.B. Gordon, Expert Opin. Biol. Ther. 22 (2022) 1489–1502. doi: 10.1080/14712598.2022.2132143
M. Abramowicz, G. Zuccotti, J.M. Pflomm, J. Am. Med. Assoc. 318 (2017) 2487–2488. doi: 10.1001/jama.2017.18515
D. Singh, Curr. Drug Ther. 19 (2024) 275–278. doi: 10.2174/0115748855274998231113110529
J.E. Hawkes, M. Al-Saedy, N. Bouche, et al., Dermatol. Clin. 42 (2024) 365–375. doi: 10.1016/j.det.2024.02.006
L.J. Scott, C.J. Dunn, K.L. Goa, Am. J. Clin. Dermatol. 2 (2001) 95–120. doi: 10.2165/00128071-200102020-00008
G. Li, D. He, X. Cai, et al., Eur. J. Med. Chem. 250 (2023) 115195. doi: 10.1016/j.ejmech.2023.115195
B.C. Du, M. Luo, C.Y. Ren, et al., Future Med. Chem. 15 (2023) 1185–1207. doi: 10.4155/fmc-2023-0101
P.H. Schafer, F. Truzzi, A. Parton, et al., Cell. Signal. 28 (2016) 753–763. doi: 10.1016/j.cellsig.2016.01.007
G.M. Keating, Drugs 77 (2017) 459–472. doi: 10.1007/s40265-017-0709-1
E.L. Crowley, M.J. Gooderham, Pharmaceutics 16 (2023) 23. doi: 10.3390/pharmaceutics16010023
P. Schafer, Biochem. Pharmacol. 83 (2012) 1583–1590. doi: 10.1016/j.bcp.2012.01.001
D. Wu, X. Zheng, R. Liu, et al., Acta Pharm. Sin. B 12 (2022) 1351–1362. doi: 10.1016/j.apsb.2021.09.027
Q. Zhou, M. Le, Y. Yang, et al., Acta Pharm. Sin. B 13 (2023) 1180–1191. doi: 10.1016/j.apsb.2022.09.023
X.N. Wu, Q. Zhou, Y.D. Huang, et al., Acta Pharm. Sin. B 12 (2022) 3103–3112. doi: 10.1016/j.apsb.2022.02.012
F.C. Meotti, F.C. Missau, J. Ferreira, et al., Biochem. Pharmacol. 72 (2006) 1707–1713. doi: 10.1016/j.bcp.2006.08.028
M. Comalada, D. Camuesco, S. Sierra, et al., Eur. J. Immunol. 35 (2005) 584–592. doi: 10.1002/eji.200425778
M. Kciuk, N. Garg, S. Dhankhar, et al., Pharmaceuticals 17 (2024) 701. doi: 10.3390/ph17060701
S. Yu, H. Yan, L. Zhang, et al., Molecules 22 (2017) 299. doi: 10.3390/molecules22020299
W. Huang, C. Liu, F. Liu, et al., Cell Biochem. Funct. 38 (2020) 249–256. doi: 10.1002/cbf.3443
Z. Chen, Y. Shi, F. Zhong, et al., Chin. Chem. Lett. 36 (2025) 109956. doi: 10.1016/j.cclet.2024.109956
X.Y. Lu, L. Kuai, F. Huang, et al., Nat. Commun. 14 (2023) 6767. doi: 10.1038/s41467-023-42477-y
Figure 1 The PDE4D inhibitory screening for the Chinese medicine library led to the discovery of P. orientalis. (A) The process of discovering P. orientalis and isolating FLDs. (B) HPLC analysis of P. orientalis-EA and FLDs. (C) The chemical structures of compounds 1–5.
Figure 2 (A–C) The binding profiles of 4, 5, 2 with PDE4 were tested by MST tests and the fitted Kd values were obtained. (D) The binding pattern of 4 with PDE4 from the crystal structure as we recently reported (PDB: 8YLC). (E, F) The putative binding patterns of 5 and 2 with PDE4 from the docking results.
Figure 3 AMF or FLDs effectively inhibited hyperproliferation and inflammation in vitro. (A) Schematic illustration of the cell experimental design. (B) Cell counting kit-8 (CCK-8) assay showing the cell proliferative viabilities of different groups. (C) Quantitative real-time polymerase chain reaction (RT-qPCR) results for the inflammatory factors IL-1α, IL-1β, IL-6, and IL-8 at 24 h Data are presented as means ± standard error of mean (SEM) (n = 3 independent experiments). **P < 0.01, ****P < 0.0001.
Figure 4 AMF and FLDs effectively alleviated the psoriasis dermatitis in vivo. (A) Schemes of the IMQ-induced psoriasiform mouse model. (B) Representative images of lesions on day 7. (C–E) Pachynsis, desquamation, and erythema of the dorsal skin were scored daily from 0 to 4. (F) The cumulative score, PASI score, as the sum of erythema, scale, and thickness scores. (G) The body weight of mice. Data are presented as means ± SEM (n = 8 independent experiments).
Figure 5 AMF and FLDs effectively increased cAMP and decreased the expression levels of several hallmark markers in psoriasis mice. (A) Enzyme linked immunosorbent assay (ELISA) quantification of cAMP. (B–E) ELISA quantification for the inflammatory factors of TNF-α, IL-6, IL-17A and IL-23. (F, G) Representative images of HE staining and the quantification of stratum corneum. Scale bar: 20 µm. (H, I) Representative images and the quantification of immunohistochemistry for CD3+. Scale bar: 50 µm. (J, K) Representative images and the quantification of immunohistochemistry for TNF-α. Scale bar: 50 µm. Data are presented as means ± SEM (n = 8 independent experiments). P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.
Figure 6 The 30% FDLs are non-irritating, safe, and nontoxic to both mice and New Zealand rabbits. (A, B) Representative images of the major organs and organ-to-body ratios in mice. Data are presented as means ± SEM (n = 3 independent experiments). P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. (C) Schematic illustration of the rabbit's experiment design. (D) Photos of rabbits' skin on day 13 of drug administration and on day 27 after two weeks of recovery. (E) HE staining of major organs of rabbits after 28 days. Rows 1–4 correspond to the following groups: Damaged skin control, damaged skin 30% FLDs 2 g/d, damaged skin 30% FLDs 5 g/d, and normal skin 30% FLDs 5 g/d, respectively. Scale bar: 2 mm for heart and kidney; 500 µm for liver, spleen, lung, and skin.
Table 1. Inhibition activity of the P. orientalis extracts and compounds against PDE4D.
| Extract/compound | PDE4D inhibitory rate (%) | IC50 (µmol/L) | |
| 1 µg/mL | 0.2 µg/mL | ||
| P. orientalis-MeOH | 90.7 | 42.7 | n.s.b |
| P. orientalis-PE | 89.3 | 26.9 | n.s.b |
| P. orientalis-EA | 95.0 | 56.4 | n.s.b |
| P. orientalis-BtOH | 35.4 | 11.6 | n.s.b |
| P. orientalis-H2O | 17.0 | 1.9 | n.s.b |
| Myricitrin (1) | 6.5 | 1.8 | 40.0 ± 1.1 |
| Quercitrin (2) | 0.4 | 1.7 | 10.0 ± 0.7 |
| Afzelin (3) | 15.4 | 7.8 | 35.8 ± 0.4 |
| AMF (4) | 102.5 | 89.7 | 0.012 ± 0.001 |
| Hinokiflavone (5) | 79.1 | 13.5 | 0.773 ± 0.102 |
| FLDs | 105.4 | 74.2 | n.s.b |
| Roliprama | 56.2a | n.s.b | 0.590 ± 0.050 |
| a Positive control, at a concentration of 800 nmol/L. b Activity was not tested. |
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