Female Albino Mice Research Articles

Chemoprotective Effect of Eugenol on Repeated dose Doxorubicin, Induced Genotoxic Lesions in Mouse Bone Marrow

In present study, an attempt has been made to evaluate the possible in vivo chemoprotective potential of eugenol against doxorubicin induced genotoxic lesion in bone marrow. Swiss albino female mice were administered Eugenol (10 mg/kg/day, orally) 15 days before doxorubicin administration as well as concomitantly with doxorubicin. Genotoxic lesions were induced by a repeated dose intraperitoneal injection of doxorubicin (5mg/kg b.w. i.p. upto 9 days (alternate day). Micronuclei assay and COMET assay were carried out to determine genetic damage in bone marrow. Histopathological evaluation of bone marrow was also done to study lesions at cellular level. The study results demonstrated that eugenol significantly mitigated Doxorubicin induced micronuclei formation and DNA damage in the bone marrow niche. Histopathological observations revealed that Doxorubicn-intoxication resulted in massive structural impairment of bone marrow which was reduced by eugenol administration. Amelioration by eugenol is more significant in mice those received eugenol 15 days prior to Doxorubicin administration suggesting its chemoprotection. The present study suggests eugenol has the promising chemoprotective effect against Doxorubin-induced genetic lesions in mice bone marrow.

Toxicopathological and Biochemical Effects of Acrylonitrile on albino female mice reproductive system

Toxicopathological and Biochemical Effects of Acrylonitrile on albino female mice reproductive system

Evaluation of the hepatoprotective effect of curcumin alone or in combination with vitamin C in methotrexate-induced hepatotoxicity in mice.

To assess the hepatoprotective effect of curcumin and/or vitamin C in methotrexate-induced hepatotoxicity. The experimental study was conducted at the Department of Pharmacology, College of Medicine, and the Iraqi Centre for Cancer and Medical Genetic Research, Mustansiriya University, Baghdad, Iraq, from Nov 12, 2020, to June 1, 2021, and comprised Swiss albino female mice aged 3-4 months and weighing 30-40g each. The mice were divided into 5 groups and treated for 10 days. Group 1 received distilled water, group 2 received single-dose methotrexate on the 10th day of the trial, group 3 was treated with curcumin plus methotrexate, group 4 was treated with vitamin C plus methotrexate, and group 5 was treated with curcumin and vitamin C plus methotrexate. Parameters measured were serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and lactate dehydrogenase, as well as hepatic tissue malondialdehyde, superoxide dismutase and glutathione. Data was analysed using SPSS 16. There were 35 mice; 7(20%) in each of the 5 groups. Hepatoprotection produced by curcumin as reflected by a decrease in lactate dehydrogenase and malondialdehyde levels was significant (p<0.05). Vitamin C also produced a significant hepatoprotection, demonstrated by a decrease in alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase and malondialdehyde levels. The combination of curcumin and vitamin C reflected an additive effect demonstrated by a significant decrease in malondialdehyde (p<0.05). Curcumin and/or vitamin C provided hepatoprotection against methotrexate-induced hepatotoxicity through modulation of oxidative stress biomarkers.

Neurobehavioral toxicity of Cold plasma activated water following oral gavage in mice

Cold plasma-activated water (PAW) is a novel technology that was recently used in biomedical research; Despite its potential, PAW's safety remains inadequately assessed. The study explores the impact of PAW on behavioral responses and brain tissue histopathology in mice. Ten-week-old female albino mice were divided into three groups each containing 10 mice (5 replicates, 2 mice/cage) and received either distilled water (DW), or distilled water exposed to cold atmospheric plasma (CAP) for 3 min (PAW-3), or 15 min (PAW-15) by oral gavage in a dose of 200 μL/mice (3 times/week) for four weeks. PAW exhibited altered physicochemical properties compared to DW. Mice exposed to PAW demonstrated reduced burrowing activity, marble burying ability, and novel object recognition compared to controls, indicating potential neurobehavioral alterations. PAW-treated groups displayed notable histological lesions in brain tissues, including nerve cell necrosis, vascular congestion, and Purkinje cell degeneration, confirming neurotoxic effects. Positive reactions for NF-κB and iNOS in brain tissues of PAW-treated mice corroborated the histopathological findings, suggesting neuroinflammation and oxidative stress. The study highlights the need for further investigation into PAW's safety profile and optimal treatment protocols to mitigate potential neurobehavioral toxicity in biomedical research.

Coenzyme Q10 ameliorates chemotherapy-induced cognitive impairment in mice: a preclinical study.

Among the three most used anticancer drugs, cyclophosphamide, Adriamycin, and 5-Fluorouracil (CAF), the most significant outcome is chemobrain, caused by increased oxidative stress, inflammatory insult, and mitochondrial dysfunction. In this study, endogenous antioxidant coenzyme Q10 (CoQ10) was evaluated for its neuroprotective effects in CICI. The chemobrain was induced in Swiss albino female mice by administering CAF (40 + 4 + 25mg/kg) intraperitoneal (i.p.) in three cycles (single injection per week) followed by treatment with CoQ10 (40mg/kg; p.o.) for up to 3weeks followed by behavioral, biochemical, molecular and histopathological analysis. Treatment with CoQ10 significantly improved cognition by improving exploring time in novel objects recognition test followed by increasing the time spent in the target quadrant in MWM test as compared to CAF-treated animals. Moreover, CoQ10 demonstrated antioxidant properties by reducing the expression of LPO while increasing levels of GSH, SOD, and catalase as compared to CAF-treated animals. While the levels of AChEs were significantly reduced after CoQ10 treatment in CAF-treated animals. In terms of its mechanism, it effectively counteracted the pro-inflammatory substances (TNF-α and IL-1β) triggered by CAF while also enhancing the levels of anti-inflammatory markers (IL-10 and Nrf2). Moreover, CoQ10 showed mitochondrial enhancers and it improved the level of Complex (I, II, and IV). Besides that, mitochondrial morphological analysis was done by TEM, and neuronal morphology along with quantification analysis was performed by H&E staining using Image J software to confirm the neuroprotective effect of CoQ10 over CAF-induced cognitive impairment. This study suggests CoQ10 can protect the mitochondria by imposing antioxidant, and anti-inflammatory properties, which could be a potential therapy for CICI.

Histopathological Changes in Kidney Tissues of Mice as Result of an Ibuprofen Drug Treatment

Ibuprofen, a non-steroidal anti-inflammatory drug, is frequently prescribed in children for diverse therapeutic indications, including fever, postoperative pain, tumors, and inflammatory disorders. The objective of this study was to investigate the changes that may occur in kidney tissue in association with prolonged administration and overdose treatment of Ibuprofen. 20 female albino mice were used. They were divided into four groups, group (I) included 5 animals and served as a control group, group (II) included 10 animals and received daily recommended therapeutic dose of Ibuprofen 2.75ul/kg body weight for ten weeks, group (III) included 10 animals and received a daily overdose of Ibuprofen 5.5ul/kg body weight for ten weeks and group (IV) included 10 animals and treated exactly as a group (II) then the animals were left for recovery for six weeks. At the end of each period, the animals were sacrificed and kidneys were excised. The drug-induced many histopathological changes in kidneys included inflammatory cellular infiltration, cloudy swelling, hydropic degeneration, hemorrhage, dilatation and congestion of blood vessels, and fibers deposition. The study concluded that Ibuprofen treatment may cause different injuries in the renal tissue of mice. After six weeks of recovery, the renal changes persist, animals may need a longer period for complete recovery.

Design and Optimization of Sesamol Nanosuspensions to Potentiate the Anti-Tumor Activity of Epirubicin against Ehrlich Solid Carcinoma-Bearing Mice.

There is a growing interest in discovering natural sources of anti-cancer drugs. Sesamol (SES) is a phenolic compound with antitumor effects. The present study aimed to investigate the anticancer properties of SES and its nano-suspensions (SES-NS) combined with Epirubicin (EPI) in breast cancer (BC) using mice bearing a solid Ehrlich tumor. The study involved 35 female albino mice and investigated the effects of SES and EPI on tumor growth, proliferation, apoptosis, autophagy, angiogenesis, and oxidative stress. Methods including ELISA, qRT-PCR, and immunohistochemistry were utilized. The findings revealed reductions in tumor growth and proliferation using SES either alone or combined and evidenced by decreased AKT (AKT Serine/Threonine kinase1) levels, angiogenesis indicated by lower levels of VEGFR (vascular endothelial growth factor), and apoptosis demonstrated by elevated caspase3 and BAX levels. Furthermore, autophagy increased and was indicated by increased levels of beclin1 and lc3, along with decreased oxidative stress as evidenced by elevated TAC (total antioxidant capacity) and reduced MDA (malondialdehyde) levels. Interestingly, SES-NS demonstrated more significant effects at lower doses. In summary, this study underscores the potential of SES as a promising agent for BC treatment. Moreover, SES-NS potentiated the beneficial effects of EPI while mitigating its adverse effects.

The Analgesic and Anti-inflammatory Properties of Caffeine Co-administration with Nefopam in Mice

This study aimed to evaluate the analgesic properties of nefopam and the adjuvant effects of caffeine. It also investigated the anti-inflammatory effect of co-administering nefopam and caffeine on Prostaglandin E2 level (PGE2). The study involved 56 female albino mice (Mus musculus), divided into seven groups, eight mice per each group. Group A which served as the control group received distilled water; Group B received 30 mg/kg BW of nefopam orally; Group C received 28.5 mg/BW of nefopam and 5 mg/BW of caffeine orally; Group D received 27 mg/BW of nefopam and 10 mg/BW of caffeine orally; Group E received 25.5 mg/BW of nefopam and 15 mg/BW of caffeine orally; Group F received 24 mg/BW of nefopam and 20 mg/BW of caffeine orally; Group G received 22.5 mg/BW of nefopam and 25 mg/BW of caffeine orally. The nociceptive response was assessed using the formalin test, showing a significant (P&lt;0.05) reduction in pain response (accumulative time of flinching and licking) was the first phase (0-5 minutes) in Group E as well as, a significant (P&lt;0.05) decrease in nociceptive response in flinching and licking in second phase (20-60 minutes) was observed in Group D. However, the Prostaglandin level was significantly (P&lt;0.05) lower in Group C. The study concluded that adding low dosages of caffeine to analgesics can boost pain relief in smaller quantities. Caffeine co-administration with nefopam may exert

Neuro-protective and redox potential of troxerutin against cypermethrin-induced neurotoxicity and oxidative stress in mice

The present study was designed to evaluate the protective efficacy of troxerutin against cypermethrin-induced behavioral defects, motor function abnormalities, and oxidative stress in mice. Twenty-four adult female albino mice were randomly divided into four equal groups. The first group served as control, the second group was treated with cypermethrin (20 mg/kg b.w) intraperitoneally at day 21, and the remaining two groups were orally supplemented with TRX (150, 300 mg/kg b.w) for 20 days and with cypermethrin (20 mg/kg b.w) intraperitoneally at day 21. Behavior activities recorded after cypermethrin exposure showed significantly impaired motor function (p≤0.05) as evidenced by the beam balance and pole test. The cypermethrin was also found to cause significant memory dysfunction. Moreover, the oxidative stress in terms of increased tissue malondialdehyde level (p≤0.05) was recorded in the cypermethrin group. The antioxidant activities of catalase and glutathione peroxidase were decreased (p≤0.05) after cypermethrin exposure. Troxerutin supplementation significantly improved the cypermethrin- -induced motor impairment and memory dysfunction. The supplementation of troxerutin significantly restored the redox status. Troxerutin attenuates the neurotoxic and behavioral deficits caused by cypermethrin. Furthermore, troxerutin also provides significant protection against cypermethrin-induced oxidative stress by improving the oxidative stress markers.

Morphological and Histopathological Liver Abnormalities Caused by Carbamazepine-Induced Injury in Female Albino Mice

Background: The adverse effects of drugs can damage various organs, especially the liver, leading to a hepatic injury known as hepatotoxicity. Drug-induced liver injury (DILI) is challenging nowadays because of the large number of different drugs used, one of the offending medications that cause DILI is carbamazepine (CBZ), since the liver has an array of functions including detoxification, it will deal with several damages caused by exposure to the drugs. Objective: investigate the effect of (CBZ) 20mg/kg/day on female mice liver after 14 and 30 days of treatment on morphological and histopathological levels. Materials and methods: 20mg/kg/day of CBZ was administered orally for (14) days to (10) female mice, another (10) mice were taking the same concentration for 30 days, and control groups were administered tap water. Results: The findings showed that CBZ can cause liver enlargement, changes in liver appearance, distortion in Glisson’s capsule, cytologic alterations, hepatocyte hypertrophy, ballooning degeneration, pyknosis, karyolysis, karyomegaly, sinusoids dilation, increase in the number and sizes of Kupffer cells, fibrosis, glycogen depletion, and cirrhosis. Conclusion: These findings have shown that carbamazepine (CBZ) can cause hepatotoxicity that can manifest into morphological and histopathological changes.

Effects of Oral Zinc Supplementation on Early Embryonic Development and Neonates of Aged Female Albino Mice

Female reproductive aging is a normal phase of life that eventually leads to menopause and reproductive senescence. The current experimental investigation was intended to study zinc supplementation effects on early embryonic development and neonates in 26-28 weeks old female mice. In this investigation, 80 mature female mice were used that were divided into two groups of forty each. Two control groups received distilled water, while two Zn groups were given 0.115 mg/kg/day Zn orally daily during 2-3 estrous cycles. The female mice were all mated with adult males. Twenty female mice from both the control and Zn groups were euthanized by CO2 gas inhalation, and then a longitudinal incision in the abdomen of each female mouse was performed and uterine horns and oviducts were detached from the body in order to obtain two-cell embryos. On the other hand, 20 pregnant mice from each group were permitted to complete their pregnancy until birth and then their neonates were collected for macroscopic examination. The findings showed that the Zn supplementation significantly (P≤0.01) improved the mean embryonic development and the quality of 2-cell stage embryo grade A. Whereas, it decreased the mean embryonic development of 2-cell stage embryo grade D in aged female mice significantly (P≤0.01) in comparison with aged control groups. Also, the count and quality of neonates from Zn-treated aged female mice enhanced significantly (P≤0.01) as compared to non-treated aged female mice. It was concluded from these findings that the Zn can improve embryonic development and neonate count and quality in aged mice.

Dioon rzedowskii: An antioxidant, antibacterial and anticancer plant extract with multi-faceted effects on cell growth and molecular signaling

This study investigated the antioxidant, anticancer, antibacterial properties of Dioon rzedowskii extract, which had not been previously explored. We aimed to determine the extract's effect on liver and breast cancer cell lines and on solid Ehrlich carcinoma (SEC) mouse model to investigate the underlying molecular mechanisms. Three female albino mice groups were established: a tumor control group, a group treated with 100 mg/kg of the extract (D100), and a group treated with 200 mg/kg of the extract (D200) for 16 days after tumor development. Results showed that the D. rzedowskii extract inhibited cell growth in both MCF-7 and HepG2 cells in a concentration-dependent manner. This was achieved by suppressing the cell proliferation and inducing apoptosis. The extract also improved liver, heart, and kidney functions compared to the tumor control. Furthermore, oral administration of the extract reduced tumor volume and alleviated oxidative stress in tumor tissue. The anticancer effects were associated with overexpression of p53 and Bax and downregulation of cyclin D1 expression, which was attributed to decreased phosphorylated MAPK kinases. Additionally, D. rzedowskii exhibited antibacterial activity against K. pneumoniae isolated from cancer patients. The extract inhibited bacterial growth and reduced the membrane integrity. The study suggests that D. rzedowskii has promising potential as an adjunctive therapy for cancer treatment. Further investigations are needed to explore its combined anticancer efficacy. These results emphasize the value of natural products in developing compounds with potential anticancer activity and support a paradigm shift in cancer management to improve patients' quality of life.

Chitosan and Grifola Frondosa nanoparticles insulate liver dysfunction in EAC-bearing mice.

Ehrlich ascites carcinoma (EAC) is a rapidly growing and undifferentiated tumor that can prompt oxidative stress and liver toxicity, whereas chitosan and Grifola Frondosa have widely recognized biological qualities. Therefore, our study designed to assess the potential ameliorative ability of chitosan nanoparticles (CS NPs) and Grifola Frondosa nanoparticles (GF-loaded casein NPs) on EAC-induced hepatic injury in mice. A total of 60 female albino mice were segregated into 6 groups (10 mice each), G1, control group; G2, CS NPs group; G3, GF-loaded casein NPs group; G4, EAC group; G5, EAC treated with CS NPs; G6, EAC treated with GF-loaded casein NPs. According to the findings, EAC considerably increased serum activities of ALT, AST, ALP as well as LDL, cholesterol, and triglycerides levels coincided with marked decrease in albumin and total protein content in liver tissue. At the same time, it drastically lowered GSH levels and catalase activity while significantly elevating MDA levels. In addition, EAC caused DNA damage and apoptosis by decreasing Bcl-2 while increasing p53 expressions. However, either CS NPs or GF-loaded casein NPs therapy improved liver architecture and functioning, increased antioxidant parameters, and prevented hepatocyte death in EAC mice. Our findings concluded that CS NPs and GF-loaded casein NPs have insulating functions against EAC-induced hepatic damage in mice.

Antitumor activity and targeting p53-PUMA mRNA expression by 5-flurouracil PLGA-lipid polymeric nanoparticles in mouse mammary carcinomas: comparison to free 5-flurouracil

Polymeric poly (lactic-co-glycolic acid) (PLGA)-lipid hybrid nanoparticles (PNPs)-based therapy are powerful carriers for various therapeutic agents. This study was conducted to evaluate the chemotherapeutic potential of free 5-flurouracil (5FU) and synthetized 5FU-PNPs and impact on p53-dependent apoptosis in mammary carcinomas (MCs) grown in mice. Breast cancer cells were injected in Swiss albino female mice and 2 bilateral masses of MC were confirmed after one week. Mice were distributed to five experimental groups; Group 1: MC control group. Groups 2 and 3: MC + free 5FU [5 or 10 mg per kg] groups. Groups 4 and 5: synthetized MC+ 5FU-PNPs [5 or 10 mg per kg] groups. Medications were administered orally, twice weekly for 3 weeks. Then, tumors were dissected, and sections were stained with hematoxylin-eosin (HE) while the other MC was used for measuring of cell death and inflammatory markers. Treatment with 5FU-PNPs suppressed the MC masses and pathologic scores based on HE-staining. Similarly, greater proapoptotic activity was recorded in 5FU-PNPs groups compared to free 5FU groups as shown by significant upregulation in tumoral p53 immunostaining. The current results encourage the utility of PNPs for improving the antitumor effect of 5FU. The chemotherapeutic potential was mediated through enhancement of tumoral p53-mediated p53 up-regulated modulator of apoptosis (PUMA) genes. Additional studies are warranted for testing the antitumor activity of this preparation in other mouse models of breast cancer.

Toxicological effects of dimethlybenzeneanthracene in Balb C mice and pharmacological intervention by silk sericin-conjugated silver nanoparticles.

Polycyclic aromatic hydrocarbons (PAHs) such as 7, 12-dimethylbenzneanthracene (DMBA), due to long-term bioaccumulation cause serious physiological processes and behavioral dysfunctions such as cancer, ageing, and hypertension. Silk sericin (SS) is instrumental in cancer applications due to presence of flavonoids and carotenoids which are natural pigments, present in the layer of sericin that has antioxidant and antityrosinase activity. It reduces oxidative stress and suppresses cancer cytokines while interacting with reactive oxygen species (ROS) to stand against lipid peroxidation. Recent research was focused to calculate the pharmacological intervention of sericin-conjugated silver nanoparticles (S-AgNO3 NPs) against DMBA-induced toxicity. For this purpose, SS protein was extracted from silkworm cocoons by degumming process and the prepared S-AgNO3 NPs via a green synthesis. In female albino mice, a total of 50 mg/kg oral administration of DMBA was used for the induction of toxicity which required almost 8 to 10 weeks approximately. After 60 days of experimentation, mice were dissected, blood samples were collected for further hematological and biochemical analysis and were euthanized via cervical dislocation. There was a significant rise in the level of red blood cells, platelets, lymphocytes, and hemoglobin at the highest applied concentration of sericin and its nanoparticles. Similarly, a reasonable decline was observed in the level of white blood cells, neutrophils, eosinophils, and monocytes as compared to the cancer-inducing group. The level of glutathione, lactate dehydrogenase, and alkaline phosphatase as well as immunoglobulins such as immunoglobulin A (IgA), immunoglobulin G (IgG), and immunoglobulin M (IgM) were significantly reduced in all treatment groups as compared to the DMBA-induced group. Substantial effects were demonstrated in response to S-AgNO3 NPs II (T) at the highest concentrations (200 mg/kg, BW) as follows: glutathione (2.42 ± 0.26 μmol/L), lactate dehydrogenase (493.6 ± 5.78 U/L), alkaline phosphatase (158.4 ± 6.35 U/L), IgA (4.22 ± 0.19 g/L), IgG (70 ± 1.70 g/L), and IgM (4.76 ± 0.12). The histopathological study of the liver, kidneys, and brain revealed that the DMBA-induced group showed cytotoxic effects against all selected organs of mice that were recovered by treatment of selective compounds but highly effective recovery was seen in S-AgNO3 NPs II (T). These results concluded that silk S-AgNO3 NPs showed significant pharmacological potential against cancer-inducing toxicity.

The Inhibitory Effect of Geraniol on CCL4-induced Hepatorenal Toxicity in Pregnant Mice through the PI3K/AKT Signaling Pathway.

Hepatotoxicity caused by CCL4 is well known. Geraniol (GNL) has high antioxidant effect that can induces liver regeneration. However, the protective effect of GNL effect on CCL4-induced hepatorenal toxicity in pregnant mice has not yet been studied. To investigate whether GNL could protect against oxidative stress induced by CCL4 via the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, which is regulated by phosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT), and has been found to have protective effects on renal and hepatic tissues. Forty-eight female albino mice weighing 25-30 g were randomly allocated to 4 groups: Group I served as a control; Group II received a toxicity-inducing single dose of 15 μL of CCL4 on the 4th day after mating; Group III received 40 mg/kg GNL + CCL4 (with GNL from the 1st day of assimilation to delivery); and Group IV received GNL alone from the 1st day of assimilation to the end of the delivery period. GNL was evaluated for its protective effects on hepatotoxicity in CCL4-treated pregnant mice. Litter size, weight, survival rate, and resorption were recorded. In addition, H & E staining was done for liver and kidney pathology as well as biochemical markers and oxidative markers malondialdehyde, superoxide dismutase, and catalase were analyzed. CCL4 significantly reduced survival rate and increased resorption after exposure. Alanine transaminase and aspartate aminotransferase concentrations in the serum, tissue MDA, blood urea nitrogen, and creatinine were increased after CCL4 exposure. GNL improved enzyme and antioxidant levels and prevented CCL4-induced hepatic injury in mice. Caspase-3 cleavage was decreased by GNL, which increased PI3K, phosphorylated AKT, Nrf2, and B-cell lymphoma 2. GNL demonstrates a protective effect against CCl4-induced hepatorenal toxicity, mediated through the activation of the PI3K/AKT signaling pathway and the upregulation of Nrf2. These findings highlight the potential therapeutic implications of GNL in mitigating oxidative stress and inflammation in liver and kidney tissues.

Antagonistic Effects of Chinese Salt and Folic Acid on Developing Swiss Albino Mice

One of the most often utilized taste enhancer in commercial meals is monosodium glutamate (MSG) commonly called Chinese salt. MSG utilization has been increasing over time and linked with toxicity in liver and other organs. Objective: To determine the teratogenic and toxic effects of Chinese salt and folic acid on developing mice. Methods: In this study, 20 female pregnant albino mice were divided into four groups, each consisted 5 mice. The control group was supplied with water. To check the teratogenicity and toxicity of Chinese salt and folic acid the treated groups such as Group-I, Group-II and Group-III were supplied with Chinese salt and/or folic acid of concentration 7.50 ug/g of their body weight. The dose was administered orally on daily basis during 6th to 12th day of gestation. This was accomplished through an 18 days trial. On the eighteenth day of gestation, the pregnant mice underwent dissection and the fetuses were retrieved. Fetuses were taken from all groups for histopathological findings and morphometry. Results: Vast range of morphological, morphometric and histological abnormalities in mice were observed in pregnant mice and fetuses. Conclusions: The findings of this study clearly revealed that Chinese salt and folic acid overdose are potentially toxic to liver and stomach.

Does Fried Street Food (Kokor) affect Lipid Profiles and bodyweight? The Finding from Swiss Albino Mice

Background: Foods fried in palm oil on the streets change the oil composition and produce toxic byproducts. Even though the health implications of fried street food are not fully understood, Ethiopians frequently consume these items. Therefore, this study evaluated the impact of street kokor fried in palm oil on mice's lipid profiles and body weight. Methods: The experiment involved 32 Swiss Albino male and female mice, which were randomly separated into four groups with equal male and female subgroups. The experimental groups, Group II, Group III, and Group IV, got 10%, 20%, and 30% of the daily food intake, respectively. In contrast, the control group (Group-I) received only pellets and a vehicle (water). The mice were killed at the end of the sixth weeks after recieving a diethyl ether anesthetic. Once their blood was drawn through a heart puncture, lipid profile tests were performed on it. Results: In this experiment, the amount of street kokor cooked in palm oil had a significant impact on the mice' body weight [F (3, 24) = 13.841, p = 0.001] and all of the mice in the experimental groups had significantly lower body weights than the mice in Group I (the control group) (P 0.05). Similarly, the dose of palm oil fried street kokor had a significant effect on serum triglyceride (TG) [F (3, 24) = 17.72, p = 0.001], serum low-density lipoprotein (LDL) [F (3, 24) = 90.344, p = 0.001], serum high-density lipoprotein (HDL) [F (3, 24) = 25.38, p = 0.001] and serum total cholesterol (TC) level of the mice [F (3, 24) = 257.480, p = 0.001]. The experimental group mice's lipid profiles, except serum HDL level, were increased significantly compared with the control group mice (P &lt; 0.05). Conclusion: Mice's body weight fell and serum lipid profiles were affected by palm oil-fried street kokor. This study found that palm oil-fried street kokor dramatically decreased mice's body weight. Furthermore, ingesting kokor cooked in palm oil significantly and proportionally elevated mice's serum lipid profiles (TG, LDL, and TC), but it also dramatically and inversely decreased HDL levels.

Camptothecin structure simplification elaborated new imidazo[2,1-b]quinazoline derivative as a human topoisomerase I inhibitor with efficacy against bone cancer cells and colon adenocarcinoma

Camptothecin is a pentacyclic natural alkaloid that inhibits the hTop1 enzyme involved in DNA transcription and cancer cell growth. Camptothecin structure pitfalls prompted us to design new congeners using a structure simplification strategy to reduce the ring extension number from pentacyclic to tetracyclic while maintaining potential stacking of the new compounds with the DNA base pairs at the Top1-mediated cleavage complex and aqueous solubility, as well as minimizing compound-liver toxicity. The principal axis of this study was the verification of hTop1 inhibiting activity as a possible mechanism of action and the elaboration of new simplified inhibitors with improved pharmacodynamic and pharmacokinetic profiling using three structure panels (A-C) of (isoquinolinoimidazoquinazoline), (imidazoquinazoline), and (imidazoisoquinoline), respectively. DNA relaxation assay identified five compounds as hTop1 inhibitors belonging to the imidazoisoquinolines 3a,b, the imidazoquinazolines 12, and the isoquinolinoimidazoquinazolines 7a,b. In an MTT cytotoxicity assay against different cancer cell lines, compound 12 was the most potent against HOS bone cancer cells (IC50 = 1.47 μM). At the same time, the other inhibitors had no detectable activity against any cancer cell type. Compound (12) demonstrated great penetrating power in the HOS cancer cells' 3D-multicellular tumor spheroid model. Bioinformatics research of the hTop1 gene revealed that the TP53 cell proliferative gene is in the network of hTop1. The finding is confirmed empirically using the gene expression assay that proved the increase in p53 expression. The impact of structure simplification on compound 12 profile, characterized by the absence of acute oral liver toxicity when compared to Doxorubicin as a standard inhibitor, the lethal dose measured on Swiss Albino female mice and reported at LD50 = 250 mg/kg, and therapeutic significance in reducing colon adenocarcinoma tumor volume by 75.36 % after five weeks of treatment with compound 12. The molecular docking solutions of the active CPT-based derivative 12 and the inactive congener 14 into the active site of hTop1 and the activity cliffing of such MMP directed us to recommend the addition of HBD and HBA variables to compound 12 imidazoquinazoline core scaffold to enhance the potency via hydrogen bond formation with the major groove amino acids (Asp533, Lys532) as well as maintaining the hydrogen bond with the minor groove amino acid Arg364.

Evaluation of antioxidant, anti-inflammatory, anticancer activities and molecular docking of Moringa oleifera seed oil extract against experimental model of Ehrlich ascites carcinoma in Swiss female albino mice

The current research intended to evaluate the antitumor properties of Moringa oleifera oil extract (MOE). Fifty-six female Swiss albino mice were employed in this study. Animals were assigned into four groups: control (C) group, moringa oil extract (MOE) group administered (500 mg/kg b. wt) MOE daily via gavage, Ehrlich ascites carcinoma (EAC) group and EAC group administered daily with (500 mg/kg b.wt) MOE for two weeks (EAC/MOE). The results showed that MOE significantly ameliorated the EAC increase in body weight and reduced the EAC cell viability. In addition, they upgraded the levels of hepatic and renal functions, inflammatory cytokines, oxidative stress markers and EAC-induced hepatic and renal histopathological changes. Treatment of EAC with MOE induced antitumor, anti-inflammatory and antioxidant effects and normalized most of the tested parameters besides the histopathological alterations in both renal and hepatic tissues. HPLC for the MOE identified Cinnamic acid, Ellagic acid, Quercetin, Gallic acid, Vanillin and Hesperidin as major compounds. The molecular docking study highlighted the virtual binding of the identified compounds inside the GSH and SOD proteins, especially for Quercetin which exhibited promising binding affinity with good interactive binding mode with the key amino acids. These results demonstrate that the antitumor constituents of MOE against EAC induced oxidative stress and inflammation by preventing oxidative damage and controlling EAC increase.