Hamster Buccal Pouch Research Articles

Effect of Indigofera aspalathoides on the Expression of Inducible Nitric Oxide Synthase During 7,12-Dimethylbenz[a]anthracene-Induced Hamster Buccal Pouch Carcinogenesis

Effect of Indigofera aspalathoides on the Expression of Inducible Nitric Oxide Synthase During 7,12-Dimethylbenz[a]anthracene-Induced Hamster Buccal Pouch Carcinogenesis

PLGA-Loaded Nedaplatin (PLGA-NDP) Inhibits 7,12-Dimethylbenz[a]anthracene (DMBA) Induced Oral Carcinogenesis via Modulating Notch Signaling Pathway and Induces Apoptosis in Experimental Hamster Model.

The present study is designed to evaluate the nanotherapeutic efficacy of prepared PLGA-loaded Nedaplatin (PLGA-NDP) against 7,12-dimethyl benz(a)anthracene (DMBA)-induced experimental oral carcinogenesis in hamster buccal pouch (HBP) model. The buccal pouch of golden Syrian hamsters was painted with 0.5% DMBA in liquid paraffin three times a week for 14 weeks, ultimately leading to the development of oral squamous cell carcinoma (OSCC). Oral administration of PLGA-NDP (preinitiation) and Cisplatin delivery (5 mg/kg b.wt) started 1 week before the carcinogen exposure and continued on alternative days. Post-administration of PLGA-NDP (5 mg/kg b.wt) started 2 days after carcinogen (DMBA) induction until the end of the experiment. After the 14th week, we observed that DMBA-painted hamsters exhibited tumor formation, morphological alterations, and well-differentiated OSSC in addition to the responsive molecular proteins during oral carcinogenesis. Furthermore, immunoblotting analysis demonstrated that PLGA-NDP inhibits Notch signaling, as evidenced by downregulation of Bcl-Xl, Bcl-2, p21, PGE2, HGF, and CXCL12 proteins, and upregulation of p53 and Bax. This apoptotic response is crucial for PLGA-NDP to induce apoptosis. In addition, RT-PCR results showed that PLGA-NDP nanoparticles play a downregulatory role in the therapeutic action of the notch signaling gene (Notch1, Notch 2, Hes1, Hey1, and Jagged1) at the mRNA transcription level in HBP carcinoma. Taken together, these data indicate that PLGA-NDP is a potent inhibitor of oral carcinogenesis and the expansion of cells that specifically target the Notch signaling pathway indicates that obstructing Notch signaling could potentially serve as a new and innovative therapeutic approach for oral squamous cell carcinoma (OSCC).

Therapeutic efficacy of axitinib as anti-angiogenesis and nivolumab as immunotherapy on DMBA induced hamster buccal pouch carcinoma utilizing vascular endothelial growth factor

Therapeutic efficacy of axitinib as anti-angiogenesis and nivolumab as immunotherapy on DMBA induced hamster buccal pouch carcinoma utilizing vascular endothelial growth factor

Estimating Anticancer Effects of Yohimbine in DMBA-Induced Oral Carcinogenesis Hamster Model: Utilizing Biochemical and Immunohistochemical Techniques.

Yohimbine is a potent bioactive indole alkaloid, isolated from a variety of biological sources and has long been used as a natural stimulant and aphrodisiac, particularly to treat erectile dysfunction. However, some literature also points toward its anticancer effect in different experimental models. The current study aimed to address a clinical concern on the therapeutic utilization of yohimbine as a repurposed drug. We employed 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch carcinogenesis model juxtaposed with biochemical investigation of several detoxification and antioxidant markers, such as Cyt p450, Cyt b5, thiobarbituric acid reactive substance (TBARS), glutathione (GSH), glutathione reductase (GR), glutathione S transferase (GST), DT-diaphorase, vitamin C, vitamin E, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). The immunohistochemical assessment of cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), proliferating cell nuclear antigen (PCNA), and cyclin D1 expression were also performed to observe the effect of yohimbine on these markers. The hamsters treated with DMBA presented the growth of tumors in the buccal pouches, accompanied by significant changes in the liver and buccal mucosa levels of Phase I & II detoxification enzymes and lipid peroxidation (LPO). A significant rise in the range of 2- to 3.5-fold was observed in Cyt p450, Cyt b5, and LPO in DMBA-treated animals. However, oral administration of yohimbine significantly restored the LPO, antioxidant, and detoxifying enzyme activities. Additionally, the levels of COX-2, IL-6, PCNA, and cyclin D1 were also found to be downregulated by yohimbine treatment. In conclusion, yohimbine improved the biochemical and immunohistochemical markers of DMBA-induced oral cancer and reverted to near normal values via ameliorating the underlying inflammation and oxidative stress conditions. Our study highlighted the potential of yohimbine as anticancer agent, especially against oral cancer and suggested its possible use as repurposed drug.

Efficacy of Different Doses of Quercetin against Chemically Induced Oral Squamous Cell Carcinoma in Hamsters

Abstract Background: The use of Caspase-3 to evaluate the chemopreventive effect of quercetin on experimentally induced squamous cell carcinoma was applied in the current study. Materials and Methods: Five groups of Syrian male hamsters were employed in the study. Group I (negative control): 5 animals do not receive any treatment. Group II: 5 animals receiving (quercetin only at a concentration of 150 mg/kg). Group III (dimethylbenz(a)anthracene [DMBA]-treated group for 14 weeks): 10 animals were coated with 0.5% DMBA. Group IV (DMBA + quercetin 150 mg/kg): 15 animals receiving quercetin of a concentration (150 mg/kg) every day through a gavage tube along with painting the hamster buccal pouch with DMBA (0.5%) three times per week for 14 weeks. Group V (DMBA + quercetin 50 mg/kg): 15 animals receiving quercetin of concentration (50 mg/kg) every day through a gavage tube along with painting the hamster buccal pouch with DMBA (0.5%) for 14 weeks at three times each week. Results: Group III showed the lowest mean area percent (10.23), whereas Group V revealed the highest mean area percent value (23.64). All groups showed a statistically significant difference among them. Conclusion: Quercetin showed apoptotic potential validated by Caspase-3, so it may be a valuable chemopreventive agent antagonizing DMBA-induced carcinogenesis in animal models.

Tumour volume and s-phase fraction analysis in induced hamster buccal pouch carcinoma utilizing cetuximab immunotherapy.

Tumour volume and s-phase fraction analysis in induced hamster buccal pouch carcinoma utilizing cetuximab immunotherapy.

The Protective Effect of Sanggenol L Against DMBA-induced Hamster Buccal Pouch Carcinogenesis Induces Apoptosis and Inhibits Cell Proliferative Signalling Pathway.

Oral squamous cell carcinoma (OSCC) has a poor prognosis when treated with surgery and chemotherapy. Therefore, a new therapy and preventative strategy for OSCC and its underlying mechanisms are desperately needed. The purpose of this study was to examine the chemopreventive effects of sanggenol L on oral squamous cell carcinoma (OSCC). The research focused on molecular signalling pathways in 7,12-dimethylbenz(a)anthracene (DMBA)-induced hamster buccal pouch (HBP) carcinogenesis. The purpose of this study was to look at the biochemical and chemopreventive effects of sanggenol L on 7,12-dimethylbenz(a)anthracene (DMBA)-induced HBP (hamster buccal pouch) carcinogenesis via cell proliferation and the apoptotic pathway. After developing squamous cell carcinoma, oral tumours continued to progress leftward into the pouch 3 times per week for 10 weeks while being exposed to 0.5 % reactive DMBA three times per week. Tumour growth was caused by biochemical abnormalities that induced inflammation, increased cell proliferation, and decreased apoptosis. Oral sanggenol L (10 mg/kg bw) supplementation with cancer-induced model DMBApainted hamsters prevented tumour occurrences, improved biochemistry, inhibited inflammatory markers, decreased cell proliferation marker expression of tumour necrosis factor-alpha (TNF- α), nuclear factor (NF-κB), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and induced apoptosis. Sanggenol L could be developed into a new medicine for the treatment of oral carcinogenesis.

The Neem Limonoid Nimbolide Modulates Key Components of the DNA Damage Response Signalling in Cellular and Animal Models of Oral Squamous Cell Carcinoma

Deregulated DNA damage response (DDR) network is implicated in cancer progression and therapy resistance. The present study was designed to investigate whether nimbolide, an anticancer neem limonoid, targets key components of the DDR signalling pathway in cellular and animal models of oral squamous cell carcinoma (OSCC). OSCC cells (SCC-4 and SCC-9), 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch (HBP) carcinoma model, chemoresistant OSCC patient-derived xenograft (PDX) model established in athymic nude mice, and tissue sections from patients with oral premalignant/malignant disease were used for the study. Key molecules that orchestrate the DDR, including the MRN complex, ATM, DNA-PKcs, H2AX, and p53, were analysed by qRT-PCR, immunoblotting, immunofluorescence, and immunohistochemistry. Cell proliferation and apoptosis indices were evaluated. Nimbolide significantly reduced 8-oxodG levels, expression of MRN, ATMS1891, and γ-H2AX, with an increase in p-p53S15 in OSCC cells as well as in the HBP model. Nimbolide potentiated the effect of KU-55933 in ATM inhibition. In the PDX model, nimbolide suppressed tumor formation, stimulated DDR and apoptosis, inhibited cell proliferation, and enhanced sensitivity to cisplatin. Analysis of p-ATM expression revealed a significant increase during the sequential progression of hamster and human OSCC. This study provides compelling evidence that nimbolide functions as a DDR inhibitor in cellular and hamster OSCC models and as a DDR activator in the PDX model primarily by targeting ATM. Small molecules like nimbolide that modulate DDR are of immense benefit in cancer therapy. The study has also unveiled p-ATM as a promising biomarker of tumour progression in human OSCCs.

High fructose Corn Syrup recast glucose transporter-5, Wnt, NF-κB signalling and mitochondrial apoptosis in an animal model of oral oncogenesis

BackgroundWnt signalling pathway, is mediated by members of T-cell factor (TCF) transcription factors family, is essential for the control of epithelial cell proliferation and death. Glucose transporter-5 (GLUT5), fructose-specific transporter, is also important in allowing transcellular fructose uptake. The goal of this work to determine how the High fructose Corn Syrup (HFCS) affected Wingless-related integration site (Wnt) and Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling in the 7,12 –dimethylbenzaanthracene (DMBA)-induced hamster buccal pouch carcinogenesis (HBPCs) model. MethodsFour groups of hamsters were created. For 12 weeks, 0.5 % DMBA was applied 3 times/week to the left side buccal pouches of the hamsters in groups (2 & 4). Additionally, the animals in groups (3 & 4) were given through drinking water of HFCS 25 %. The control animals were from group 1. By using western blot analysis, signalling network markers of the GLUT-5, Wnt, TCF-4, GSK-3β and NF-κB as well as mitochondrial apoptotic pathway marker expression B-cell lymphoma protein 2 (Bcl-2)-associated X (Bax) and cyclooxygenase – 2 (COX-2) was assessed. ResultsDrinking water uptake of 25% HFCS encouraged progress of HBP carcinomas by constitutive stimulating of the Wnt pathway via GSK-3β overexpression. HFCS suppressed Wnt signalling which contributed the NF-κB attenuation and changes the signalling markers in apoptotic network. ConclusionsOur hypothesis suggests a mechanically crosstalk between Wnt and NF-κB signalling pathways in HBP carcinomas that is developed by HFCS. HFCS that targets the Wnt pathway and its downstream signalling mediators could be additive reason for cancer development.

Allicin (diallylthiosulfinate) Restores the Altered Lipid Profile, Erythrocyte Fragility and Permeability in 7,12-dimethylbenz(a)anthracene-induced Hamster Buccal Pouch Carcinogenesis

Allicin (diallylthiosulfinate) Restores the Altered Lipid Profile, Erythrocyte Fragility and Permeability in 7,12-dimethylbenz(a)anthracene-induced Hamster Buccal Pouch Carcinogenesis

Serum Raman spectroscopy: Evaluation of tumour load variations in experimental carcinogenesis.

Several serum Raman spectroscopy (RS) studies have demonstrated its potential as an oral cancer screening tool. This study investigates influence of low tumour load (LTL) and high tumour load (HTL) on serum RS using hamster buccal pouch model of experimental oral carcinogenesis. Sera of untreated control, LTL, and HTL groups at week intervals during malignant transformation were employed. Serum Raman spectra were subjected to multivariate analyses-principal component analysis, principal component-based linear discriminant analysis (for stratification of study groups), and multivariate curve resolution-alternating least squares (MCR-ALS) (to comprehend biomolecular differences). Multivariate analysis revealed misclassifications between LTL and HTL at all week intervals. MCR-ALS components showed statistically significant abundances between control versus LTL and control versus HTL, but could not discern LTL and HTL. MCR-ALS components exhibited spectral mixtures of proteins, lipids, heme and nucleic acids. Thus, these findings support use of serum RS as a screening tool as varying tumour load is not a confounding factor influencing the technique.

Assessment of DNA ploidy on experimentally induced hamster buccal pouch carcinoma (Histological and flow cytometric studies)

Assessment of DNA ploidy on experimentally induced hamster buccal pouch carcinoma (Histological and flow cytometric studies)

Usnic acid attenuates 7,12-dimethylbenz[a] anthracene (DMBA) induced oral carcinogenesis through inhibiting oxidative stress, inflammation, and cell proliferation in male golden Syrian hamster model.

In this study, we investigated the chemopreventive efficacy of usnic acid (UA), an effective secondary metabolite component of lichens, against 7,12-dimethylbenz[a]anthracene (DMBA)-induced oral squamous cell carcinoma (OSCC) in the hamster model. Initially, the buccal pouch carcinogenesis was induced by administering 0.5% DMBA to the HBP (hamster buccal pouch) region about three times a week until the 10th week. Then, UA was orally treated with different concentrations (25, 50, 100 mg/kg b.wt) on alternative days of DMBA exposure, and the experimental process ended in the 16th week. After animal experimentation, we observed 100% tumor incidence with well-differentiated OSCC, dysplasia, and hyperplasia lesions in the DMBA-induced HBP region. Furthermore, the UA treatment of DMBA-induced hamster effectively inhibited tumor growth. In addition, UA upregulated antioxidant levels, interfered with the elevated lipid peroxidation by-product of thiobarbituric acid reactive substances, and changed the activities of the liver detoxification enzyme (Phase I and II) in DMBA-induced hamsters. Furthermore, immunohistochemical staining of inflammatory markers (iNOS and COX-2) and proliferative cell markers (cyclin-D1 and PCNA) were upregulated in the buccal pouch part of hamster animals induced with DMBA. Notably, the oral administration of UA significantly suppressed these markers during DMBA-induced hamsters. Collectively, our findings revealed that UA exhibits antioxidant, anti-inflammatory, antitumor, and apoptosis-inducing characteristics, demonstrating UA's protective properties against DMBA-induced HBP carcinogenesis.

Therapeutic potential of epigallocatechin-3-gallate on cancer stem cells of DMBA induced hamster buccal pouch carcinoma

Therapeutic potential of epigallocatechin-3-gallate on cancer stem cells of DMBA induced hamster buccal pouch carcinoma

Effect of Thymoquinone on Skeletal Muscle Regeneration and Innervation in Induced Degeneration of the Hamster Buccal Pouch

Effect of Thymoquinone on Skeletal Muscle Regeneration and Innervation in Induced Degeneration of the Hamster Buccal Pouch

The potential preventive effect of dietary phytochemicals In Vivo

IntroductionChemoprevention refers to using specific substances during oncogenesis. Curcumin and catechins are both polyphenol types of phytochemicals present in curcuma longa and green tea. The effect of curcumin is synergistic with epigallocatechin gallate, the most abundant polyphenol in tea.AimTo evaluate and compares the chemopreventive effect of both green tea and curcumin (each individually and in combination) through induction of hamster buccal pouch carcinoma.Materials and methodsSquamous cell carcinoma was chemically induced in fifty Syrian golden hamsters divided into 5 groups (10 each). The first group was used as a normal control group. The second group received the carcinogenic agent only. The other three groups received green tea, curcumin, and a combination of both, respectively. Flow cytometry, immunofluorescence, and immunohistochemical assays were used to evaluate apoptosis, proliferation, and angiogenesis. ANOVA test was used to analyze the results between the study groups.ResultsThe cells of the positive control group (B) resulted in 11.57% apoptosis. In the study groups, treatment of the cells with green tea (C), and curcumin (D) and both of them (E) showed increased apoptosis. The fluorescent image in group B showed an increase of the red fluorescence in the nucleus and cytoplasm of the squamous cell carcinoma cells while groups C, D, and E showed a decrease of the red fluorescence in the nuclei of the squamous cell carcinoma cells. The microvessel density was higher in the positive control group as compared to the treated groups.ConclusionsThe combination of green tea and curcumin has a significant chemopreventive effect against oral carcinogenesis.

Anti-dysplastic Effect of Nettle Extract and Its Nano-formulation on 7,12-Dimethylbenz[a]anthracene Induced Hamster Buccal Pouch Carcinogenesis

Anti-dysplastic Effect of Nettle Extract and Its Nano-formulation on 7,12-Dimethylbenz[a]anthracene Induced Hamster Buccal Pouch Carcinogenesis

The Correlation Between CD44 and Angiogenesis in Oral Squamous Cell Carcinoma Induced in Buccal Pouch in Syrian Hamster that Underwent Radiotherapy.

Angiogenesis with radiotherapy is a significant focus of recent studies to confirm the importance of combined treatments, as vascular control can have a great therapeutic target. Vascular endothelial growth factor is the key mediator of angiogenesis in cancer. In addition, some studies suggest the value of CD44 as a potential early marker of angiogenesis. Investigating the expression of vascular endothelial growth factor (VEGF) and CD44 in oral squamous cell carcinoma (OSCC) after inducing it in hamsters then undergoing radiotherapy and comparing outcomes before and after therapy to verify changes of these markers. an experimental study consisted of 18 samples of OSCC which induced in right buccal pouch of hamsters (group1) and 18 samples of OSCC which induced in the same way and were exposed to radiation therapy (group2), Biopsies were taken and fixed with formalin, paraffin waxed in conventional H&E and immunostained with monoclonal anti-VEGF and anti-CD44. our findings didn't reveal a statistically significant difference in the expression of VEGF(p =0.342) and CD44 (p=0.187) between group1 & group 2. moreover, we found tumor cells which weren't affected and resistant to radiotherapy, also revealed positive expression of VEGF & CD44, otherwise, we noticed Pearson coefficient was a significant correlation that indicated to a moderate relation. cancerous cells that showed a high expression of these markers, give elevated radiosensitivity and resist the treatment. Subsequently, we assure the importance of applying anti-VEGF and/or anti-CD44 as a supportive therapy with radiation therapy.

Chemopreventive efficacy of honokiol on experimentally induced hamster buccal pouch squamous cell carcinoma

chemopreventive efficacy of honokiol on experimentally induced hamster buccal pouch squamous cell carcinoma

Serum Raman spectroscopy in experimental carcinogenesis hamster buccal pouch model: Exploring early diagnostic capability

AbstractAbout two third of oral cancer cases present at advanced stages, emphasizing the need for screening tools for early diagnosis. Raman spectroscopy (RS) can prove an appropriate tool for early diagnosis as biochemical changes occur before morphological changes. Due to limitations with study of early oral cancer stages in human subjects, we performed a sequential carcinogenesis study in animal model. In the present study, we aim to probe early biochemical changes occurring during DMBA induced oral carcinogenesis in hamster buccal pouch model, using serum RS (SRS). Serum being systemic biofluid can reflect the true in vivo state, is minimally invasive and offers advantages of remote diagnosis and serial sampling. The female Syrian golden hamsters were treated with 0.5% DMBA and retro‐orbital blood collection was performed every week for a period of 14 weeks. An increase in classification efficiency as the DMBA treatment progressed, with distinct classification of >70% seen as early as week 5 (W5), appreciably early to development of visual changes (W8–W10) was observed. Furthermore, the early treatment weeks (W1–W4) and healthy condition (W0) show no misclassifications with weeks exhibiting frank tumours (W9–W14), demonstrating efficacy of SRS to stratify healthy versus carcinogen exposure. The findings suggest that as oral carcinogenesis progresses, biochemical alterations in serum such as increasing protein and loss of lipid content can be detected by RS, highlighting the feasibility and utility of SRS in early oral cancer diagnosis. To our knowledge, this is the first study exploring the ex vivo sequential approach to gain insights into oral cancer progression.