Tectoridin Research Articles

Tectoridin inhibits the growth of bladder cancer by regulating PI3K/MAPK pathway through RAB27B.

Bladder cancer (BC) is a common and malignant tumor of the urinary tract, and its treatment options are limited. Tectoridin (TEC) has antitumor activity against prostate and colon cancer, but its effects on BC are poorly understood. BC cells were treated with increasing concentrations of TEC, and its effects on cell proliferation, migration, invasiveness, and apoptosis were assessed. Xenograft mouse model was used to evaluate the influences of TEC on BC tumor growth. Western blot analysis was conducted to explore the downstream pathways affected by TEC. TEC treatment decreased BC cell viability in a dose-dependent manner (IC50 ≈ 25 μM), and inhibited cell proliferation, migration, and invasiveness while promoting apoptosis. Clinical analysis revealed high expression of RAB27B in BC tumor tissues, particularly in advanced stages, correlating with an unfavorable prognosis. In vitro experiments demonstrated that TEC suppressed the PI3K/MAPK pathway by targeting RAB27B, and overexpression of RAB27B counteracted the antitumor effects of TEC. In xenograft models, TEC administration suppressed tumor growth, reduced tumor volume, inhibited cell proliferation, and suppressed the PI3K/MAPK pathway, highlighting its potential as an inhibitor of tumor growth. TEC suppresses BC tumor growth by targeting RAB27B and inactivating the PI3K/MAPK signaling and may provide a promising therapeutic target for BC treatment.

Impact of tectoridin on the pharmacokinetics of florfenicol via targeting cytochrome P450 and P-glycoprotein of rats

Belamcanda chinensis (L.) DC, commonly used with florfenicol in Chinese veterinary clinics for respiratory tract infections, contains the major effective isoflavone, tectoridin (TEC). This study aimed to investigate the impact of TEC co-administration on the pharmacokinetics of florfenicol in vivo. Male rats received oral TEC (50 mg/kg BW) or sterile water for seven days, followed by a single oral dose of florfenicol (25 mg/kg BW) on the 8th day. Non-compartmental methods analysed the pharmacokinetics of florfenicol, while real-time reverse transcription polymerase chain reaction (RT-PCR), Western blot, and immunohistochemical analyses measured expression levels of cytochrome P450 (CYP) isoforms in the liver and P-glycoprotein (P-gp) in the jejunum. TEC significantly decreased florfenicol’s AUC(0–∞), MRT(0–∞), t 1/2z, Vz/F, and C max by 24.75%, 18.43%, 55.47%, 43.05%, and 19.48%, while increasing CLz/F by 33.33%. TEC also up-regulated hepatic CYP1A2 and CYP3A1 mRNA expression, as well as intestinal MDR1, by 1.39-fold, 1.85-fold, and 1.65-fold. This coincided with a respective increase in protein expression by 1.37-fold, 1.39-fold, and 1.43-fold. These findings suggest that TEC-induced alterations in the pharmacokinetics of florfenicol may be attributed to increased CYP and P-gp expression. Further investigations are warranted to understand the implications of these findings on the clinical effectiveness of florfenicol in veterinary practice.

Tectoridin inhibits the progression of colon cancer through downregulating PKC/p38 MAPK pathway.

Colon cancer is one of the most familiar malignancies worldwide, with high morbidity and high mortality. This study intended to explore the role and mechanism of tectoridin (TEC) in regulating the progression of colon cancer. First, colon cancer cell lines (HCT116 and SW480 cells) were treated with different doses of TEC (0-200μM). Then, CCK8 and clone formation experiments were performed to detect cell proliferation. Flow cytometry and western blot were conducted to examine apoptosis. Subsequently, Transwell assay and wound-healing test was employed to determine the effect of TEC on colon cancer cell invasion and migration. Next, western blot was performed to monitor the PKC/p38 MAPK pathway activation. In addition, a tumor model was established in nude mice to explore the effect of TEC on tumor growth in vivo. TEC dose-dependently dampened the proliferation, migration and invasion of colon cancer cells and facilitated their apoptosis. In addition, TEC abated the tumor cell growth in vivo. Besides, TEC dose-dependently suppressed the expression of PKC and p38 MAPK. Moreover, inhibiting the PKC pathway almost cancel out the anti-tumor effects induced by TEC. TEC attenuates the colon cancer progression by inhibiting the PKC/p38 MAPK pathway.

A novel strategy to evaluate the quality of herbal products based on the chemical profiling, efficacy evaluation and pharmacokinetics

The purpose of this study was to establish a chemical profiling method to compare the chemical composition of herbal products by using extracts of Belamcandae Rhizoma(EBR) extracted with different polarity solvent as an example, and evaluate the quality of EBR based on the analysis of chemical profiling, efficacy evaluation and pharmacokinetics. As seen from the results of chemical profiling, the PCA and PLS-DA score plot indicated that the dots of Belamcandae Rhizoma water extracts were separated from ethanol extracts obviously, which suggested significant differences of chemical profiling existing in the different solvent extracts. The PCA and PLS-DA loading plot illustrated that the main compounds contributing to chemical profiling differences were tectoridin(TD), iristectorin B(IT B), iridin(ID), tectorigenin(TG), irigenin(IG), iristectorigein A(IG A), dichotomitin(DT) and irisflorentin(IF). Furthermore, the results of HPLC analysis demonstrated that the contents of these main compounds in ethanol extracts were significantly higher than that in water extracts (P < 0.01). Both the pharmacological and hematoxylin-eosin staining studies indicated that the ethanol extracts of Belamcandae Rhizoma had a better therapeutic effect than water extracts in oral ulcer model rats (P<0.01). It is suggested that the ethanol extracts were beneficial to the absorption and bioavailability of TG which was one of the most important bioactive compounds of Belamcandae Rhizoma in pharmacokinetic study in rats. This work provided a novel method to optimize the extraction process of EBR and related herbal products. Compared with the conventional chemical fingerprint methodology, the approach proposed above is not only a powerful tool to identify efficacy-related components for the quality evaluation, but also can be used to predict the therapeutic efficacy of herbal products.

Tectoridin isolated from Belamcanda chinensis (L.) DC. exerts an estrogenic effect through extracelullar signal-regulated kinase (ERK)-dependent pathway

Phytoestrogens are naturally occurring chemicals deriving from plants with a structure similar to estrogen [1]. Tectorigenin (TG) and its glycoside tectoridin (TD) are isoflavonoids isolated from the rhizome of Belamcanda chinensis (L.) DC. It is reported that they trigger estrogenic activities via classical estrogen receptor (ER)-mediated signaling pathway. However, TG and TD showed a moderate and almost no binding affinity to both ERα and ERβ, respectively. These binding affinities to ERs were much lower than that of genistein (GE), a famous phytoestrogen [2, 3]. On the other hand, TG and TD at 10µM strongly induced luciferase activity in MCF-7 cells transfected with estrogen responsive element (ERE) containing construct. These ERE transactivations were as potent as that of GE, and TD showed even more pronounced ERE transactivation compared to TG in spite of their wretched bindings to ERs. We also confirmed the proliferation abilities of TG and TD in MCF-7 cells by using colongenic assay and cell cycle analysis. After serum starvation period, TG and TD increased the cell population to 21.3% and 19.6% at S phase, respectively, after 4 days treatment while vehicle control cells only remained to 4.4%. In order to elucidate the molecular mechanism of an estrogenic effect of TD, we measured the TD-induced ERE transactivation in the presence of MAPKs, PKA, PKC inhibitors (SP600125, SB203580, U0126, SQ22536, GF10923X) in MCF-7 cells. The TD-induced ERE transactivation was significantly inhibited by only ERK inhibitor, U0126. In conclusion, TD stimulated proliferation and S-phase entry in hormone starved MCF-7 cells, and its estrogenic effect could be exerted through ERK-dependent pathway.