Asian Pacific Journal of Tropical Biomedicine

Number 14(2), 2024

47-54
Catalpa bignonioides extract improves exercise performance through regulation of growth and metabolism in skeletal muscles

Authors: Jeong, Hoibin; Lee, Dong-joo; Kwon, Sung-Pil; Park, SeonJu; Kim, Song-Rae; Kim, Seung Hyun; Park, Jae-Il; Lee, Deug-chan; Choi, Kyung-Min; Lee, WonWoo; Park, Ji-Won; Yun, Bohyun; Cho, Su-Hyeon; Kim, Kil-Nam

Abstract

View in PDF

Number of views: 9

Objective: To evaluate the effects of Catalpa bignonioides fruit extract on the promotion of muscle growth and muscular capacity in vitro and in vivo. Methods: Cell viability was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell proliferation was assessed using a 5-bromo-2’-deoxyuridine (BrdU) assay kit. Western blot analysis was performed to determine the protein expressions of related factors. The effects of Catalpa bignonioides extract were investigated in mice using the treadmill exhaustion test and whole-limb grip strength assay. Chemical composition analysis was performed using high-performance liquid chromatography (HPLC). Results: Catalpa bignonioides extract increased the proliferation of C2C12 mouse myoblasts by activating the Akt/mTOR signaling pathway. It also induced metabolic changes, increasing the number of mitochondria and glucose metabolism by phosphorylating adenosine monophosphate-activated protein kinase. In an in vivo study, the extract-treated mice showed improved motor abilities, such as muscular endurance and grip strength. Additionally, HPLC analysis showed that vanillic acid may be the main component of the Catalpa bignonioides extract that enhanced muscle strength. Conclusions: Catalpa bignonioides improves exercise performance through regulation of growth and metabolism in skeletal muscles, suggesting its potential as an effective natural agent for improving muscular strength.

55-64
Icariin plus curcumol enhances autophagy through the mTOR pathway and promotes cathepsin B-mediated pyroptosis of prostate cancer cells

Authors: Wang, Xu-Yun; Xu, Wen-Jing; Li, Bo-Nan; Sun, Tian-Song; Sheng, Wen

Abstract

View in PDF

Number of views: 8

Objective: To examine the effect of icariin plus curcumol on prostate cancer cells PC3 and elucidate the underlying mechanisms. Methods: We employed the Cell Counting Kit 8 assay and colony formation assay to assess cell viability and proliferation. Autophagy expression was analyzed using monodansylcadaverine staining. Immunofluorescence and Western blot analyses were used to evaluate protein expressions related to autophagy, pyroptosis, and the mTOR pathway. Cellular damage was examined using the lactate dehydrogenase assay. Moreover, cathepsin B and NLRP3 were detected by co-immunoprecipitation. Results: Icariin plus curcumol led to a decrease in PC3 cell proliferation and an enhancement of autophagy. The levels of LC3-II/LC3-I and beclin-1 were increased, while the levels of p62 and mTOR were decreased after treatment with icariin plus curcumol. These changes were reversed upon overexpression of mTOR. Furthermore, 3-methyladenine resulted in a decrease in inflammatory cytokines, pyroptosis-related protein levels, and lactate dehydrogenase concentration, compared to the icariin plus curcumol group. Inhibiting cathepsin B reversed the regulatory effects of icariin plus curcumol. Conclusions: Icariin plus curcumol demonstrates great potential as a therapeutic agent for castration-resistant prostate cancer by enhancing autophagy via the mTOR pathway and promoting pyroptosis mediated by cathepsin B. These findings provide valuable insights into the molecular mechanisms underlying the therapeutic potential of icariin and curcumol for prostate cancer treatment.

65-72
Hydrangea serrata extract exerts tumor inhibitory activity against hepatocellular carcinoma HepG2 cells via inducing p27/CDK2-mediated cell cycle arrest and apoptosis

Authors: Kim, Ye-eun; Hwang, Jeonghye; Kim, Ki-Young

Abstract

View in PDF

Number of views: 7

Objective: To examine the inhibitory effect of Hydrangea serrata extract against hepatocellular carcinoma HepG2 cells and its underlying mechanisms. Methods: The effects of Hydrangea serrata extract on growth inhibition of tumor cells and spheroids were assessed using MTT and 3D culture assays. Quantitative real-time PCR and Western blot analyses were employed to investigate the changes in mRNA and protein expression levels of molecules related to cell cycle and apoptosis. Results: Hydrangea serrata extract effectively inhibited the growth of both tumor cells and spheroids. The extract also significantly upregulated p27 mRNA expression and downregulated CDK2 mRNA expression, leading to cell cycle arrest. Moreover, increased BAX/Bcl-2 ratio as well as caspase-9 and - 3 were observed after treatment with Hydrangea serrata extract, indicating the induction of tumor cell apoptosis. Conclusions: Hydrangea serrata extract has the potential to alleviate tumors by effectively modulating cell-cycle-related gene expressions and inducing apoptosis, thereby inhibiting tumor growth.

73-81
Benzydamine hydrochloride ameliorates ethanol-induced inflammation in RAW 264.7 macrophages by stabilizing redox homeostasis

Authors: Dasgupta, Tiasha; Manickam, Venkatraman

Abstract

View in PDF

Number of views: 7

Objective: To evaluate the protective effect of benzydamine hydrochloride against ethanol-induced oxidative stress and inflammation in RAW 264.7 macrophages. Methods: RAW 264.7 macrophages were treated with ethanol (100 mM) and benzydamine hydrochloride (7.5 μM). The inflammatory status was confirmed by measuring pro-(TNF-α and IL-6) and anti-inflammatory (IL-10) cytokines through ELISA and RT-PCR assays. Reactive oxygen species generation and mitochondrial membrane potential were investigated to study the protective role of benzydamine hydrochloride against ethanol-induced oxidative stress. Apoptosis detection was also investigated using flow cytometry and acridine orange/ethidium bromide staining. Results: Benzydamine hydrochloride significantly decreased the secretion of TNF-α and IL-6, as well as the generation of reactive oxygen species inside the cells, thereby stabilizing the mitochondrial membrane potential and reducing DNA fragmentation. The ethanol-induced cellular necrosis was also reversed by the administration of benzydamine hydrochloride. Conclusions: Benzydamine hydrochloride ameliorates ethanol-induced cell apoptosis and inflammation in RAW macrophages.

82-92
NUDT5 promotes the growth, metastasis, and Warburg effect of IDH wild-type glioblastoma multiforme cells by upregulating TRIM47

Authors: Zhang, Zi-Fa; Liu, Shu-Ming

Abstract

View in PDF

Number of views: 10

Objective: To explore the regulatory mechanism of NUDT5 in glioblastoma multiforme (GBM). Methods: GEPIA database was used to predict the expressions of NUDT5 and tripartite motif family proteins 47 (TRIM47) in GBM patients. RT-qPCR and Western blot analyses were performed to examine NUDT5 expression in GBM cells. LN-229 cell proliferation, migration as well as invasion were estimated by CCK-8, colony formation, wound healing, and Transwell assays following interference with NUDT5. ECAR assay, L-lactic acid kit, glucose detection kit, and ATP detection kit were applied for the detection of glycolysis-related indexes. Co-immunoprecipitation experiment was carried out to verify the relationship between NUDT5 and TRIM47. Results: GEPIA database showed that NUDT5 expression was significantly increased in GBM patients. Inhibiting the expression of NUDT5 in GBM cells significantly suppressed the viability, proliferation, invasion, migration, and glycolysis of GBM cells. Moreover, TRIM47 was highly expressed in GBM cells and interacted with NUDT5. Overexpression of TRIM47 partially reversed the inhibitory effect of NUDT5 downregulation on the proliferation, metastasis, and glycolysis of GBM cells. Conclusions: NUDT5 promotes the growth, metastasis, and Warburg effect of GBM cells by upregulating TRIM47. Both NUDT5 and TRIM47 can be used as targets for GMB treatment.