Vernodalin Alleviates Cardiotoxicity and Inflammation in Isoproterenol-Mediated Myocardial Infarction through NF-κB/AMPK Signaling Pathways in Rats.

BACKGROUND: Myocardial infarction (MI) is the foremost cause of mortality in cardiovascular diseases. MI ultimately exacerbates cardiotoxicity due to the release of toxicity biomarkers and inflammatory infiltration. AIM: Vernodalin (VN) is a renowned cytotoxic sesquiterpene lactone that possesses antioxidant, anticancer, and anti-inflammatory properties. The cardioprotective mechanism of VN remains concealed. Hence, we explored the cardioprotective efficacy of VN on isoproterenol (ISO)- mediated MI and analyzed its underlying mechanism. METHODS: Wistar albino rats were injected ISO (85 mg/kg bw) subcutaneously to induce MI to evaluate the cardioprotective potential of VN (10 mg/kg bw) by assessing heart weight/ body weight index, hemodynamic, toxicity enzymes, histopathology, inflammatory mediators, and signaling pathway. ISO enhanced heart weight/body weight index, cardiotoxicity enzymes, biomarkers, inflammation, and histopathological changes while reducing hemodynamic parameters and VEGF-B, AMPK, and eNOS signaling pathways. RESULTS: Treatment with VN could significantly (p<0.05) mitigate the heart weight/body weight index, cardiotoxicity enzymes, biomarkers, inflammatory cytokines, and histopathological changes while enhancing hemodynamic parameters and VEGF-B, AMPK, and eNOS signaling pathways. Collectively, our findings revealed that the VN ameliorated defensive action against MI and averted myocardial injury by reducing the NF-κB-mediated inflammatory pathways in rats. CONCLUSION: These findings established that VN expressively preserves the myocardium and employs anti-inflammatory actions by regulating NF-κB, VEGF-B, AMPK, and eNOS signaling pathways.

Oridonin attenuated human PC-3 cell activity by modulating the Wnt/ß-catenin signaling.

BACKGROUND: Prostate cancer (PC) prevention is effectively achieved through its inhibition. Oridonin (ORD), an active diterpenoid isolated from Rabdosia rubescens, has been shown to have an inhibitory effect on PC cells, although its impact on PC is unknown. OBJECTIVES: The present work investigated the actions and probable mechanisms of ORD on cellular proliferation, apoptosis, PC, and the wingless-type MMTV integration site family member 2 (Wnt)/ß-catenin signaling pathway using the androgen-independent PC-3 cell line. MATERIAL AND METHODS: In this study, cell viability was analyzed with MTT assay method, apoptotic morphology determined using DAPI dye method, while protein (CD1333, OCT-4, Nanog, SOX-2 & Aldh1A1) and mRNA expressions were analyzed with western blotting and real time polymerase chain reaction (PCR). RESULTS: We demonstrated a concentration-dependent ORD inhibition of PC-3 cell proliferation and inhibition of induction apoptosis. Furthermore, ORD decreased PC-3 Wnt-2, phosphorylated glycogen synthase kinase-3 (p-GSK3), and ß-catenin protein levels and downregulated cyclin-D1 and c-myc messenger ribonucleic acid (mRNA). CONCLUSIONS: Oridonin inhibited proliferation and induced apoptosis in PC-3 cells, with the findings suggesting that it acted via the Wnt/ß-catenin pathway to exert its effects. This study demonstrates that ORD may impact PC.

The protective effect of Sanggenol L against DMBA-induced hamster buccal pouch carcinogenesis induces apoptosis and inhibits cell proliferative signalling pathway.

BACKGROUND: 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. AIM: 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. METHODS: 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. RESULTS: Oral sanggenol L (10 mg/kg bw) supplementation with cancer-induced model DMBA-painted 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. CONCLUSION: Sanggenol L could be developed into a new medicine for the treatment of oral carcinogenesis.

Betanin inhibits PI3K/AKT/mTOR/S6 signaling pathway, cell growth and death in osteosarcoma MG-63 cells.

It is possible to develop new chemopreventive compounds so that cancer cells can be targeted in an exclusive manner. Bioactive natural compounds have demonstrated to be efficient chemotherapeutic agents, safe and cost-effective. Majority of anti-cancer medications are derived from natural sources, particularly of plant origins. Betanin (betanidin-5-O-ß-glucoside) is the most common betacyanin with antioxidant, anti inflammatory and anticancer properties. The present study therefore investigated the effect of betanin onosteosarcoma MG-63 cells. The mechanistic pathway of inflammatory responses, cell proliferation and apoptosis were investigated. The MG-63 cells were treated with betanin for 24 h. Betanin actions on the appearance of cell arrangements, morphological changes, ROS induced Δψm , cell migration, cell adhesion and proliferative mechanistic marker expression of PI3K/AKT/mTOR/S6were analyzed. Betanin inhibited MG-63 cells at IC50 concentrations between 9.08 and 54.49 µM and induced apoptosis by triggering the ROS mechanism. Betanin inhibited proliferation and migration of MG-63 cells and induced DNA fragmentation. Betanin also modified the key mediator expression levels of PI3K/AKT/mTOR/S6 signaling pathways. Betanin can potentially be utilized in bone carcinoma therapeutics to inhibit, reverse or delay osteosarcoma.

Protective effect of Pueraria lobata leaves on doxorubicin-induced myocardial infarction in experimental Wistar rats.

The present study intended to explore the preventive effects of Pueraria lobata leaves against doxorubicin (DOX)-induced myocardial infarction (MI) in Wistar rats. The rats were separated into four groups, with each group containing six rats. Group I control rats; group II received DOX-alone in six equivalent injections for 2 weeks; group III received DOX as abovementioned with P. lobata oral administration for 2 weeks; group IV received P. lobata alone for 2 weeks. At the end of the experiment, postcervical dislocation and MI induced by DOX were determined on the basis of the variations in the animal body and heart weight and further instabilities in cardiac marker enzymes aspartate transaminase, lactate dehydrogenase, creatine kinase, creatine kinase-myoglobin binding, and cardiac troponin I in the serum. At the same time, for group III animals, which were exposed to P. lobata, all the above-denoted marker levels were maintained. Levels of some crucial heart-binding proteins like heart fatty acid binding protein, monocyte chemoattractant protein-1, and transforming growth factor beta were elevated in DOX-alone treated rats. Additionally, group III animals treated with P. lobata showed some preventive downregulated expressions of these binding proteins. Histopathological observations also revealed the preventive effect of P. lobata. Ultimately proteins tangled in the phosphoinositide 3-kinase/protein kinase B pathway were studied by Western blot. P. lobata treatment downregulated the inflammatory markers. The findings suggest that P. lobata exhibits cardioprotective effect on MI.

Protective effect of piperlongumine on inflammation and oxidative stress against ischemia-reperfusion injury in animal kidney.

AIM: Piperlongumine (PL), an alkaloid from the Piper longum plant, is acknowledged for various biological properties. The study aimed to explore the protective effect of PL on ischemia reperfusion injury (I/R) in rat kidney. METHODS: 24 adult male Sprague-Dawley rats (200 to 250 mg) were randomly allocated to four groups (n = 6/group): Group I: sham control, Group II: (I/R) renal ischemia/reperfusion kidney renal blocked for 1hour using clamps, followed by 2hr reperfusion. Group III: PL (25 µg/kg) + I/R group and Group IV: PL (50 µg/kg) + I/R group. Rat kidneys were exposed to 60 min of two-sided deep ischemia followed by 120 min of reperfusion. PL (25 and 50 µg/kg bw) was administered intraperitoneally half an hour before the ischemia. Creatinine, urea, and few renal markers activity in serum were assessed. Oxidative stress and inflammatory markers were also evaluated. In addition, the expressions of COX-2 and eNOS in animal kidneys were tested by western blotting. RESULTS: Pre-treatment with PL in ischemia­reperfused rats significantly reduced the pathological damage in the kidney and declined the levels of serum creatinine and other renal parameters. PL treatment diminished the serum levels of TNF-α, IL-6, and IL-1ß, as well as messenger RNA expressions. Important biological defence parameters such as superoxide dismutase and glutathione levels were upregulated while malondialdehyde levels were down-regulated in PL ischemia rats. CONCLUSION: PL exhibits a protective effect against inflammation and oxidation in ischemia reperfusion animals (Fig. 5, Ref. 32).

Scutellarin alleviates cerebral ischemia/reperfusion by suppressing oxidative stress and inflammatory responses via MAPK/NF-κB pathways in rats.

Neuroinflammation contributes to the progression of cerebral ischemia/reperfusion (I/R) damage. Scutellarin (SL) is a glucuronide flavonoid that has apoptotic, anti-inflammatory, and anti-tumor properties. It is anti-oxidant and anti-inflammatory mechanism as a neuroprotective against ischemic brain injury is unknown. The purpose of the study was to examine the role and mechanism of SL in preventing I/R damage in a rat model. SL (40 and 80 mg/kg) was given to the rats for 14 days before the ischemic stroke. SL administration prevented I/R mediated brain injury, and neuronal apoptosis. Malondialdehyde, superoxide dismutase, glutathione, IL-6, and IL-1ß and nitric oxide were modulated by SL. SL suppressed the p65 and p38 expressions in particular. The findings show that SL protects rats from cerebral damage caused by I/R through the nuclear factor kappa-B p65 and p38 mitogen-activated protein kinase signaling pathway. Thus, SL protected the brain of rats from ischemic injury by inhibiting the inflammatory process.

Modulatory apoptotic effects of sinomenine on Mycoplasma pneumonia through the attenuation of inflammation via ERK/JNK/NF-κB signaling pathway.

Mycoplasma pneumoniae (MPP) induced pneumonia is a common disease of children. Sinomenine (SIN) is an isoquinoline mainly sequestered from Sinomenium acutum. It is a promising drug for treating arthritis, lung, colon, liver and gastric cancer. Hence, the present study investigated the role and mechanism of SIN treatment in MPP induced pneumonia in experimental in-vivo mice model. The BALB/c male mice were separated into four groups (n = 6 mice/group): normal, MPP, MPP + SIN (20 mg/kg bw), and SIN (20 mg/kg bw) alone. Results were expressed as mean ± SD. Data were analyzed using one way Analysis of Variance (ANOVA) with the Dunnett's post hoc test using SPSS v 18.0. P value < 0.05 was considered significant. The total protein, cell count, inflammatory cytokines, MP-IgM, Monocyte chemo attractant protein-1 (MCP-1), and MP-DNA were measured. The protein expressions of Bax/Bcl-2, ERK, JNK, NF-κB were analyzed and histopathology of lungs was examined. SIN treatment significantly (p < 0.05) reduced the total proteins, cell counts in BALF, inflammatory cytokines, MP-IgM, MCP-1, MP-DNA and reversed the histological alterations. SIN attenuated the apoptotic pathway through the modulation of Bax/Bcl-2 expression. SIN alleviated pulmonary inflammatory mediators and apoptosis in MPP-infected mice via suppression of ERK/JNK/NF-κB signaling. SIN administration diminished inflammation and lung fibrosis by inhibiting apoptosis in MPP mice. Hence, SIN is a potential natural protective remedy for MPP.

Protective effect of lupeol on arthritis induced by type II collagen via the suppression of P13K/AKT signaling pathway in Sprague dawley rats.

To explore the therapeutic value of lupeol on collagen-induced arthritis (CIA) in rats, a rheumatoid arthritis model. Lupeol is well known pentacyclic triterpene found in various plant sources, which possess anti-inflammatory and antioxidant actions. The current study was assessed the anti-arthritic potential of lupeol and its molecular mechanisms as compared with indomethacin (Indo) in collagen-induced arthritis CIA rats. The rats were randomly alienated into five groups: Control, CIA alone, CIA + lupeol (10 mg/kg bw), CIA + Indomethacin (3 mg/kg bw), and lupeol (10 mg/kg bw) alone. The paw volume, biochemical, hematological parameters, inflammatory enzymes, and cytokines were measured. As well protein expression of apoptotic proteins, and histopathological of ankle joint were examined. Inflammatory markers, cytokines, histological changes, paw volume, and inflammation were intensely reduced and enhanced apoptosis by lupeol. Alterations in hematological parameters, rheumatoid factor, C-reactive protein, and ceruloplasmin in arthritis were reverted by lupeol. Protein expressions of Bcl-2, and P13K/Akt signaling were declined, whereas the Bax, caspssae-3, and caspase-9 were elevated. These results highlighted that lupeol suppresses P13K/Akt signaling and has a promising anti-arthritic potential for collagen-induced rheumatic arthritis treatment. Hence lupeol would be suggested as an alternative natural source with potent anti-inflammatory and apoptotic actions for chronic inflammatory disorders.

Nerolidol induced apoptosis via PI3K/JNK regulation through cell cycle arrest in MG-63 osteosarcoma cells.

The aim of the present study was to determine the cell proliferation, apoptotic pathway analysis through protein, mRNA and cell cycle arrest mechanism in nerolidol induced osteosarcoma MG-63 cells. The osteosarcoma MG-63 cells were treated with various doses of nerolidol (15 and 20 µM/ml) for 24 h. Cell proliferation was examined using assist method of MTT assay, fixed the IC50 value of nerolidol 15 µM/ml. Reactive oxygen species (ROS) generation was analyzed by DCFH-DA dye, mitochondrial potential detected by Rh-123 dye, apoptotic morphological changes identified by AO/EtBr, PI, DAPI staining, and cell adhesion were detected by using fluorescence microscope. Cell proliferation, and apoptotic molecular protein and mRNA expressions such as ERK, P38, p-PI3K, p-JNK, Bcl-2, JNK, p-P38, cyclin-D1, and Bax were analyzed in osteosarcoma MG-63 cells. Nerolidol significantly suppressed the osteosarcoma cells progression in a dose dependent manner (p < .05) evident in the oxidative stress induction and apoptotic morphological changes. Nerolidol also regulated the protein PI3K/AKT mechanistically via induction of apoptosis Nerolidol suppresses osteosarcoma MG-63 cells by PI3K/AKT by cell cycle arrest at early phase of G0/G1. To sum up, nerolidol suppressed the growth of bone cancer cells and can be finally targeted as a potent drug for analyzing its chemotherapeutic effects in future.

Effects of Syringic Acid on Apoptosis, Inflammation, and AKT/mTOR Signaling Pathway in Gastric Cancer Cells.

Gastric cancer is one of the most common cancer and deadly disease worldwide. Despite substantial advances made in the treatment of gastric cancer, existing therapies still encounter bottlenecks. Chemotherapy, for instance, could lead to serious side effects, high drug resistance and treatment failure. Phytochemical-derived compounds from plants offer novel strategies as potent drug molecules in cancer therapy. Given the low toxicity and higher tolerance rate of naturally occurring compounds, the present study evaluated the effects of syringic acid on cytotoxicity, oxidative stress, mitochondrial membrane potential, apoptosis, and inflammatory responses in gastric cancer cell line (AGS). AGS cells were treated with various concentrations (5-40 µg/mL) of syringic acid for 24 h, after which cytotoxicity was analyzed. Reactive Oxygen Species (ROS), antioxidant enzyme activities, mitochondrial membrane potential (MMP, Δψ m), cell morphologies, the expression of apoptotic markers and protein expression patterns were also investigated. Results indicated that syringic acid-treated cells developed anti-cancer activities by losing MMP, cell viability, and enhancing intracellular ROS. Syringic acid selectively developed apoptosis in a dose-dependent manner via enhanced regulation of caspase-3, caspase-9 and Poly ADP-ribose Polymerase (PARP) whereas decreasing the expression levels of p53 and BCL-2. Syringic acid also lowered activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) whereas Thio Barbituric Acid Reactive Substances (TBARS) increased. Syringic acid suppressed gastric cancer cell proliferation, inflammation, and induced apoptosis by upregulating mTOR via AKT signaling pathway. The study suggests syringic acid may constitute a promising chemotherapeutic candidate for gastric cancer treatment. Our study is the first report on the anti-cancer effects of syringic acid against gastric cancer cells via apoptosis, inhibition of inflammation, and the suppression of the mTOR/AKT signaling pathway.

Inhibiting the PI3K/Akt, NF-κB signalling pathways with syringic acid for attenuating the development of oral squamous cell carcinoma cells SCC131.

OBJECTIVES: To evaluate the anti-inflammatory and antiproliferative effect of syringic acid (SRA) on oral squamous cell carcinoma (OSCC) SCC131 cells via suppression of NF-κB-induced PI3K/Akt signalling pathway. METHODS: The present study assesses the anticancer effects of SRA alongside human oral cancer (HOC) SCC131 cells through the fabrication of reactive oxygen species (ROS) and activated apoptosis. DAPI and Rh-123 staining were used to assess the apoptotic nuclear characteristic, mitochondrial membrane potential, cell adhesion and migration by fluorescence microscope with SRA treatment. KEY FINDINGS: Syringic acid inhibits cell viability (IC50 values of 25 µm), adhesion, migration and induced apoptosis. MTT assay demonstrated SRA-induced apoptotic events, inhibition of invasion and angiogenic signalling in SCC131 cell line. Furthermore, SRA treated with SCC131 cells suppresses the protein expression of inflammatory, angiogenesis and PI3K/Akt signalling pathways. It is suggested that SRA prevents the translocation of NF-κB and PI3K/Akt activated products to the nucleus, thereby suppressing angiogenesis via downregulation of vascular endothelial growth factor. CONCLUSIONS: Therefore, addition of SRA to SCC131 cells may provide a promising natural therapeutic strategy against squamous cell carcinomas with potential application in clinical analysis.

Syringic acid suppresses oral squamous cell carcinoma SCC131 cell proliferation via modulation of mitochondria-mediated apoptosis signaling pathways.

Apoptosis is an important process of cell death that controls the intrinsic and extrinsic pathways. Syringic acid (SRA)-a phenolic compound well-known in traditional Indian Ayurvedic medicine-has been reported to suppress cell proliferation of various cancer cells. Therefore, the current study aimed to investigate the inhibitory role of SRA on the proliferation of oral squamous cell carcinoma cells (SCC131) via reactive oxygen species (ROS) and induced mitochondria-mediated apoptosis. The study results showed that SRA (IC50 ) was able to induce apoptosis in SCC131 cells via increased ROS generation, alteration of mitochondrial membrane potential, nuclear fragmentation, apoptotic morphological differences, and DNA injury. Moreover, SRA inhibited proliferative markers such as proliferating cell nuclear antigen and cyclin D1 protein expression in SCC131 cells. A diminished level of B-cell lymphoma 2 (Bcl-2) and augmented level of Bcl-2-associated X protein (Bax) were considered as markers of apoptotic cell death. In addition, SRA was able to decrease Bcl-2 and increase mutant p53, caspase-9, Bax, and caspase-3 expression in SCC131 cells. Taken together, SRA succeeded in inhibiting SCC131 cell growth through the ROS and mitochondria-mediated apoptosis in oral cancer cells.

Data on efficacy of umbelliferone on glycoconjugates and immunological marker in 7,12-dimethylbenz(a)anthracene induced oral carcinogenesis.

Umbelliferone, a phenolic coumarin and dietary agent is believed to play a key role in pharmacological activities including anti-cancer and anti-oxidants effect in various in vitro and in vivo models. In present data on the pre-treatment of umbelliferone (30 mg/kg b.w.) for 16 weeks to 7,12-dimethylbenz(a)anthracene induced hamsters provides protection on cellular integrity by observing the status of cell surface glycoconjugates in the circulation and buccal mucosa and cytokeratin immunoexpression in the buccal mucosa of experimental animals. Data presented in this article brief that umbelliferone exhibits potent to clear cell surface abnormalities in buccal tissues and circulation during carcinogenesis and restored the expression of cytokeratin effect against 7,12-dimethylbenz(a)anthracene induced hamster buccal pouch carcinogenesis, which is attributes to its inhibitory role on glycoprotein synthesis or on the activity of the glycosyltransferase. In an article associates with this data set given the relevance to the research article entitled "Dose responsive efficacy of umbelliferone on lipid peroxidation, anti-oxidant, and xenobiotic metabolism in 7,12-dimethylbenz(a)anthracene-induced oral carcinogenesis" namely Vijayalakshmi and Sindhu, 2017 assessed 100% tumour formation in 7,12-dimethylbenz(a)anthracene treated hamsters and oral administration of umbelliferone at a dose of 30 mg/kg b.w to 7,12-dimethylbenz(a)anthracene treated hamsters prevents tumour incidence, restores the status of the biochemical markers in circulation and buccal mucosa and also dysregulation in the expression of molecular markers. Given the relevance to this article entitled "Berberine protects cellular integrity during 7,12-dimethylbenz[a]anthracene-induced oral carcinogenesis in golden Syrian hamsters" namely Sindhu and Manoharan 2010, which were based on spectrophotometry and florescence microscope analysis.

Umbelliferone arrest cell cycle at G0/G1 phase and induces apoptosis in human oral carcinoma (KB) cells possibly via oxidative DNA damage.

Umbelliferone (UMB) has widespread pharmacological activity, comprising anti-inflammatory, anti-oxidant, anti-genotoxic and anti-immunomodulatory but the anticancer activity remains unknown in human oral carcinoma (HOC) KB cells. MTT assay determinations was revealed that treatment of KB cells with UMB, prevent and reduce the cell proliferation with the IC50 - 200µM as well as induces loss of cell viability, morphology change and internucleosomal DNA fragmentation in a concentration dependent manner. Acridine orange and ethidium bromide dual staining assay established that UMB induced apoptosis in KB cells in a dose dependent manner. Alkaline comet assay determination revealed UMB has the potential to increase oxidative DNA damage in KB cells through DNA tail formation significantly (p<0.05). Furthermore, UMB brought a dose-dependent elevation of reactive oxygen species (ROS), which is evidenced by the DCF fluorescence, altered the mitochondrial membrane potential in KB cells. Similarly, we observed increased DNA damage stimulated apoptotic morphological changes in UMB treated cells. Taken together, the present study suggests that UMB exhibits anticancer effect on KB cell line with the increased generation of intracellular ROS, triggered oxidative stress mediated depolarization of mitochondria, which contributes cell death via DNA damage as well as cell cycle arrest at G0/G1 phase. The results have also provided us insight in the pharmacological backgrounds for the potential use of UMB, to target divergent pathways of cell survival and cell death. To conclude UMB could develop as a novel candidate for cancer chemoprevention and therapy, which is our future focus and to develop a connectivity map between in vivo and in vitro activity.

Dose responsive efficacy of umbelliferone on lipid peroxidation, anti-oxidant, and xenobiotic metabolism in DMBA-induced oral carcinogenesis.

This study evaluated the chemopreventive potential of umbelliferone (UMB) on 7,12- dimethylbenz[a]anthracene (DMBA) induced hamster buccal pouch carcinogenesis. The mechanistic pathway for chemopreventive potential of UMB was evaluated by measuring the status of tumour incidence, tumour volume, and tumour burden as well as by analyzing the status of phase I, phase II detoxification agents, lipid peroxidation, antioxidants, histopathological changes and also expression patterns of cell proliferation (PCNA, Cyclin D1) and apoptotic (p53) markers using immunohistochemistry in DMBA induced hamster buccal pouch carcinogenesis. Oral squamous cell carcinoma was created by painting of 0.5% DMBA in liquid paraffin three times a week for 14 weeks, in the golden Syrian hamsters buccal pouches. We observed 100% tumor formation with high tumor volume, tumor burden and over expression of mutant p53, PCNA, and cyclin D1 in the DMBA alone painted hamsters as compared to control hamsters. Oral administration of UMB at a dose of 30mg/kg body weight to DMBA-treated hamsters completely prevented tumor incidences and restored the status of the biochemical markers in the plasma, liver and buccal mucosa, and also prevented the deregulation in the expression of molecular markers in group 4. Therefore, the present study suggests that UMB has potent chemopreventive, anti-lipid peroxidative and antioxidant potential as well as modulating effect on phase I and phase II detoxification system with reduced cell proliferation and induced apoptosis in experimental oral carcinogenesis.

Evaluation of antioxidant and stabilizing lipid peroxidation nature of Solanum xanthocarpum leaves in experimentally diethylnitrosamine induced hepatocellular carcinogenesis.

Solanum xanthocarpum Schrad. & Wendl, is a traditional edible leaves as a form of decoction, extracts used as a herbal medicine, and consumed for health promoting profiles. The present investigation was carried out to evaluate antioxidant status and lipid peroxidation level of anticancer activity of Solanum xanthocarpum (SXC) on Diethylnitrosamine (DEN) induced hepato carcinogenesis in male Wistar albino rats. Hepatic cancer was developed on the liver of Wistar rats treated by DEN or vehicle three times a week for 16 weeks. Tumour incidence, tumour volume, tumour burden, lipid peroxidation, antioxidant, liver marker enzymes and histopathological changes were assessed in DEN alone and in DEN+SXC leaves extract treated rats. Hundred percent tumour incidences with an imbalance in carcinogen metabolizing enzymes and cellular redox status were observed in rats treated with DEN alone. Oral administration of SXC aqueous leaves extract treatment at a dose of 150mg/kg b.w. to DEN treated rats were prevented tumour incidence and restored the elevated activities of liver marker enzymes and antioxidant status to near normal with decreased lipid peroxide levels. The biochemical consistent with histopathological observations suggesting marked hepatoprotective effect of the leaves extract in a dose dependent manner. These results clearly suggest that SXC aqueous leaves extract treatment prevents liver damage, lipid peroxidation, protects the antioxidant defense system and anti-carcinogenic potential in DEN induced hepatic carcinogenesis.