Dataset Information

Arctiin Inhibits Inflammation, Fibrosis, and Tumor Cell Migration in Rats With Ehrlich Solid Carcinoma.

ABSTRACT:

Background and objectives

ESC or Ehrlich solid carcinoma is a type of tumor originating from a spontaneous mammary adenocarcinoma in mice. It is a highly aggressive and fast-growing carcinoma that can create a solid mass when inserted under the skin. Its solid, undifferentiated form makes it an ideal model for researching cancer biology, tumor immunology, and testing various anti-cancer treatments. Additionally, arctiin has multiple beneficial properties, such as anti-proliferative, anti-oxidative, anti-adipogenic, and anti-bacterial. This study aimed to explore the potential anti-cancer benefits of arctiin in rats with ESC while also analyzing its effects on cell fibrosis markers, tumor cell migration, and inflammasome pathways.

Methods

Rats were given a tumor in their left hind limb via an intramuscular injection consisting of 2×10⁶ cells. After eight days, some of the rats received a daily oral dose of 30 mg/kg of arctiin for three weeks. Muscle samples were observed under an electron microscope or stained with hematoxylin/eosin. Additionally, gene expression and protein levels of toll-like receptor 4 (TLR4), NLR family pyrin domain containing 3 (NLRP3), signal transducer and activator of transcription 3 (STAT3), transforming growth factor (TGF)-β, endothelial growth factor (VEGF), and cyclin D1 were assessed in another part of the muscle samples.

Results

When ESC rats were given arctiin as a treatment, their mean survival time increased and their tumor volume and weight decreased. Additionally, when tumor tissue was examined under an electron microscope, it showed signs of pleomorphic cells, necrosis, nuclear fragmentation, membrane damage with cytoplasmic content spilling, and loss of cellular junction. The stained sections with hematoxylin/eosin showed a dense cellular mass and compressed, degenerated, and atrophied muscle. However, treatment with arctiin improved all these effects. Finally, the expression of TLR4, NLRP3, STAT3, TGF-β, VEGF, and cyclin D1 was significantly reduced with arctiin treatment.

Conclusions

Through the use of arctiin, tumor size and weight were effectively reduced, leading to an increase in the average survival time of rats and an improvement in muscle structure. Additional research has shown that arctiin is able to suppress inflammation, fibrosis, and the migration of tumor cells by inhibiting STAT3, TGF-β1, TLR4, NLRP3, VEGF, and cyclin D1.

SUBMITTER: Alfair BM

PROVIDER: S-EPMC10495034 | biostudies-literature | 2023 Sep

REPOSITORIES: biostudies-literature

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Publications

Arctiin Inhibits Inflammation, Fibrosis, and Tumor Cell Migration in Rats With Ehrlich Solid Carcinoma.

Alfair Bayan M BM Jabarti Amirah A AA Albalawi Shyma S SS Khodir Ahmed E AE Al-Gayyar Mohammed M MM

Cureus 20230910 9

<h4>Background and objectives</h4>ESC or Ehrlich solid carcinoma is a type of tumor originating from a spontaneous mammary adenocarcinoma in mice. It is a highly aggressive and fast-growing carcinoma that can create a solid mass when inserted under the skin. Its solid, undifferentiated form makes it an ideal model for researching cancer biology, tumor immunology, and testing various anti-cancer treatments. Additionally, arctiin has multiple beneficial properties, such as anti-proliferative, anti ...[more]

PMID: 37701157

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Project description:Background and objectives Hepatocellular carcinoma (HCC) is a highly aggressive malignant tumor with a poor prognosis. It is currently the second most common cause of cancer-related mortality. Arctiin, a compound found in plants commonly used as a vegetable in Asian countries and as an ingredient in traditional European dishes, possesses various properties, including anti-proliferative, anti-senescence, anti-oxidative, anti-tumor, toxic, anti-adipogenic, and anti-bacterial effects. Our study aims to investigate the potential antitumor activity of arctiin against HCC in rats by inhibiting cell fibrosis and apoptosis. Methods Rats were induced with HCC by administering thioacetamide. Arctiin was orally administered to some rats twice a week for 16 weeks at a dose of 30 mg/kg. The liver impairment was evaluated by measuring serum α-fetoprotein (AFP) and examining liver sections stained with Masson trichrome or anti-hypoxia-induced factor-1α (HIF-1α) antibodies. The hepatic expression of messenger RNA and protein levels of HIF-1α, protein kinase C (PKC), extracellular signal-regulated kinase (ERK), β-catenin, and mothers against decapentaplegic homolog 4 (SMAD4) were analyzed. Results Our study demonstrated that arctiin can potentially increase the survival rate of rats. This is achieved through a reduction in serum AFP levels and hepatic nodules. We also observed that arctiin has the ability to inhibit the formation of fibrotic tissues and necrotic nodules in HCC rats. Additionally, arctiin can significantly decrease the expression of HIF-1α, PKC, ERK, β-catenin, and SMAD4. Conclusion Arctiin has demonstrated potential anti-tumor properties that could ameliorate HCC. Studies have shown that it may increase survival rates and reduce the number of tumors and AFP levels. Arctiin works by inhibiting HCC-induced hypoxia, thus blocking the expression of HIF-1α. It also helps to slow down tumor fibrosis by decreasing the expression of β-catenin and SMAD4. Furthermore, arctiin has been found to downregulate PKC and ERK, reducing hepatic tissue apoptosis.

Project description:Background and objectives Ehrlich solid carcinoma (ESC) is a type of tumor originating from a spontaneous mammary adenocarcinoma in mice. It is highly aggressive and fast-growing and can create a solid undifferentiated mass when inserted under the skin. This makes it an ideal model for assessing cancer biology and tumor immunology. Echinacoside is a natural phenylethanoid glycoside with anti-inflammatory, anti-endoplasmic reticulum stress, anti-oxidative stress, and other beneficial properties. This study explored the potential anti-cancer benefits of echinacoside in rats with ESC. The study also analyzed its effects on tumor cell proliferation, differentiation, motility, and inflammation. Methods The study involved injecting rats with tumors in their left hind limb using an intramuscular injection of 2×106 cells. After 14 days, some rats were given a daily intraperitoneal dose of 30 mg/kg echinacoside for three weeks. Muscle samples were then analyzed under an electron microscope. In addition, gene expression and protein levels of various factors such as phosphoinositide 3-kinases (PI3K), mammalian target of rapamycin (mTOR), hypoxia-inducible factor (HIF)-1α, cyclin D1, cyclin-dependent kinase 2 (CDK2), tumor necrosis factor (TNF)-α, and nuclear factor (NF)κB were evaluated in another part of the muscle samples. Results After being treated with echinacoside, the ESC rats experienced a significant increase in their mean survival time from 27 days to 48 days. This treatment also resulted in a decrease in the volume and weight of the tumor. Upon examining the tumor tissue under an electron microscope, signs of damage such as pleomorphic cells, necrosis, nuclear fragmentation, membrane damage with cytoplasmic content spilling, and loss of cellular junction were observed. However, the treatment with echinacoside was effective in improving these effects. Furthermore, the expression of PI3K, mTOR, HIF-1α, cyclin D1, CDK2, TNF-α, and NFκB was significantly reduced due to the echinacoside treatment. Conclusions Our research found that echinacoside has antitumor properties that resulted in a substantial decrease in tumor size and weight, leading to an increase in the average survival time of rats and an improvement in muscle structure. Additionally, echinacoside was shown to ameliorate hypoxia by suppressing HIF-1α, reduce inflammation by decreasing NFκB and TNF-α, decrease proliferation by reducing PI3K, and block cyclin D1 and CDK2 to inhibit differentiation.

Project description:Background Ehrlich solid carcinoma (ESC) is characterized by rapid proliferation and a short survival time. Because Ehrlich ascites carcinoma (EAC) resembles human cancer cells, Ehrlich solid and ascetic forms are commonly used to determine the anticancer effects of various compounds. Luteolin is a flavonoid compound found in many dietary sources, including carrots, peppers, celery, olive oil, peppermint, and oregano. Luteolin has potent anti-inflammatory, antidiabetic, antitumor, and antiapoptotic activities. Aims This study aims to investigate the antitumor activity of luteolin against ESC in rats by affecting the Wnt/β-catenin/SMAD4 pathway. Methods We introduced 0.15 ml of Ehrlich cells (2 × 106) ESC into the left hind thighs of rats. After eight days of inoculation, the rats orally received 25 mg/kg of luteolin daily. We stained sections of tumor tissues with Masson's trichrome. We used another part of the tumor tissue to assess gene and protein expression of Wnt, β-catenin, E-cadherin, and SMAD4. Results Treatment of carcinoma rats with luteolin increased the mean survival time and reduced tumor volume and weight. In addition, examination of tumor tissue stained with Masson's trichrome showed loosely to densely packed collagen fibers in between neoplastic cells and scattered papillary expansion of a loose blue band of collagen expression along the covering adipose connective tissue and extending in a fine strand in between muscle fibers, which was ameliorated by treating rats with luteolin. Finally, treating ESC in rats with luteolin overexpressed E-cadherin and downregulated Wnt, β-catenin, and SMAD4. Conclusions We found luteolin has antineoplastic activity against ESC by reducing tumor size and weight while improving the structure of muscle cells. It works by suppressing Wnt, β-catenin, and SMAD4, resulting in decreased tumor cell proliferation and differentiation. Additionally, luteolin overexpresses E-cadherin, leading to reduced tumor cell invasion and metastasis.

Project description:Background Cancer is the second-leading cause of death worldwide. According to a 2018 WHO report, 9.6 million deaths occurred globally due to cancer. Ehrlich carcinoma is characterized by rapid proliferation and a short survival time. Ligustilide is a phthalide derivative and is one of the main compounds in Danggui essential oil and Rhizoma Chuanxiong. It has many protective effects, such as anticancer, anti-inflammatory, antioxidant, and neuroprotective effects. Aims We conducted this study to investigate the antitumor activity of ligustilide against Ehrlich solid carcinoma (ESC) in rats by affecting beclin 1, mammalian target of rapamycin (mTOR), B-cell lymphoma 2 (BCL2), and 5' AMP-activated protein kinase (AMPK). Materials and methods Twenty rats were intramuscularly implanted in the thigh of the left hind limb with a 200-µL tumor cell suspension in PBS containing 2 × 106 cells. After eight days of inoculation, 10 rats out of the 20 were treated with oral 20 mg/kg ligustilide daily. At the end of the experiment, samples of muscles with ESC were separated. Sections prepared from the muscle samples with ESC were immunohistochemically stained with anti-Ki67 antibodies. Another part of the muscle samples with ESC was used to assess gene expression and protein levels of beclin 1, mTOR, BCL2, and AMPK. Results Treatment of carcinoma rats with ligustilide elevated the mean survival time and reduced tumor volume and weight. Moreover, examination of tumor tissue stained with hematoxylin/eosin showed an infiltrative, highly cell-dense mass supported by a small to moderate amount of fibrovascular stroma and intersected with multifocal myofibril necrosis. Treatment with ligustilide ameliorated all these effects in the carcinoma group without affecting the control group. Finally, treatment with ligustilide significantly decreased the expression of beclin 1, mTOR, and AMPK associated with elevated expression of BCL2. Conclusions Our study aimed to explore the potential chemotherapeutic activity of ligustilide against ESC. We found that ligustilide effectively reduced tumor size and weight, indicating its antineoplastic activity against ESC. We further investigated that ligustilide inhibits cell proliferation by suppressing Ki67 and mTOR and activates autophagy through beclin 1 activation. Moreover, ligustilide inhibits apoptosis by upregulating BCL2. Finally, ligustilide reduced the expression of AMPK, preventing its ability to promote tumor cell growth.

Dataset Information

Arctiin Inhibits Inflammation, Fibrosis, and Tumor Cell Migration in Rats With Ehrlich Solid Carcinoma.

Background and objectives

Methods

Results

Conclusions

Publications

Arctiin Inhibits Inflammation, Fibrosis, and Tumor Cell Migration in Rats With Ehrlich Solid Carcinoma.

Similar Datasets

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