Markers In Rats Research Articles

Bone strength is reduced in a neonatal androgenized rat model

BackgroundWhether polycystic ovary syndrome (PCOS) affects bone health during a woman's lifespan remains controversial. An androgenized rodent model replicated many metabolic and reproductive features of women with PCOS, and we aimed to use it to investigate the impact of androgens on microarchitecture (by micro-CT), bone mechanical strength, bone formation and resorption markers in rats with intact ovaries (SHAM) who underwent oophorectomy. MethodsWistar rats (Rattus norvegicus albinus) were employed for the experiments in this study. The protocol of androgenization consisted of the application of 1.25 mg s.c. testosterone propionate beteween days 2–5 of life, while the controls received the same amount of corn oil s.c. as previously established. Androgenized SHAM rats exhibited chronic anovulation identified by vaginal cytology and a reduction in the proportion of corpus luteum in the ovary in comparison to control SHAM rats. The realization of the ovariectomy or SHAM procedure occurred on Day 100 of life. All groups (n = 8) were followed-up for 180 days to address the study endpoints. ResultsMicro-CT from androgenized female rats (SHAM) showed a divergence between the trabecular and cortical bone profiles. Compared to SHAM controls, these rats had an increase in trabecular bone mass with a diminution in bone resorption C-terminal telopeptide of type 1 collagen (CTX) (p < 0.05), a concomitant decrease in cortical area and thickness in the femur, and a reduction in the strength of the femur on the mechanical test (p < 0.01). ConclusionsOur results suggest that a reduction in the cortical thickness and cortical area observed in PCOS model rats was associated with a reduced strength of the femur, despite increased trabecular formation. Ovariectomy in the androgenized OVX group limited the progression rate of cortical bone loss, resulting in bone resistance and cortical thickness comparable to those observed in the control OVX group.

The Effect of Interval Training on PTX3, VCAM-1, and CRP in Rats with Metabolic Syndrome

Background: Sedentary lifestyle and lack of exercise cause cardiovascular diseases and metabolic syndrome. Decreased movement in recent decades has caused cardiovascular diseases. Methods: In this research, 35 male Wistar rats weighing 220 ± 20 g were divided into 5 groups (seven rats in each group) by a simple random method. The first and second experimental groups were given 100 grams per liter of fructose with water for 6 weeks, and the third experimental group received this for 14 weeks. The training group performed the interval training protocol on the treadmill for eight weeks and 5 days a week. One-way analysis of variance (ANOVA) was used to compare the groups. Results: The use of the fructose diet for 6 weeks and 14 weeks caused metabolic syndrome in male Wistar rats. Induction of metabolic syndrome increased the plasma levels of PTX3, VACM-1, and CRP at the end of 6 weeks (P = 0.001, P = 0.018, and P = 0.004, respectively) and the fourteenth week (P = 0.001, P = 0.001, and P = 0.001, respectively). Eight weeks of interval training significantly reduced PTX3, VACM-1, and CRP (P = 0.034, P = 0.027 and P = 0.021, respectively). Conclusions: The fructose diet caused metabolic syndrome and a significant increase in inflammatory markers in rats, and high-intensity interval training significantly reduced inflammatory factors in them.

Pleurospermum candollei Methanolic Extract Ameliorates CCl4-Induced Liver Injury by Modulating Oxidative Stress, Inflammatory, and Apoptotic Markers in Rats.

The main objective of this study was to investigate the hepatoprotective potency of the Pleurospermum candollei methanol extract against CCl4-induced liver damage in rats. HPLC technique was used to estimate the presence of polyphenols in the methanol extract of P. candollei (PCM), while proximate analysis revealed the presence of carbohydrates, lipids, and moisture in the extract. The antioxidant potential of PCM was evaluated by 2,2-diphenylpicrylhydrazyl (DPPH) and reducing power assay, which showed a high percentage of inhibition against free radicals. Hepatotoxicity was induced by carbon tetrachloride (CCl4). CCl4 administration reduced the activity of endogenous antioxidants, whereas it increased the production of nitrites and hydrogen peroxide (H2O2) in rats. Furthermore, the level of hepatic markers in serum was also elevated after CCl4 administration. Moreover, the expression of stress-related markers, proinflammatory mediators, and apoptotic genes was enhanced in CCl4-treated rats. Coadministration of PCM along with CCl4 in rats reduced the levels of free radicals and the above genes to normal levels. CCl4 administration caused histopathological alterations in liver tissues, while cotreatment with PCM mitigated liver injuries. These findings suggest that the methanol extract of P. candollei possesses antioxidant and anti-inflammatory properties and can prevent liver injury. Further pharmacological research will be helpful in determining the effectiveness of P. candollei in humans. Development of FDA-approved plant-based anti-inflammatory drugs can help treat patients and reduce the chances of toxicity.

Alleviating Potential of &lt;i&gt;Zingiber officinale&lt;/i&gt; and Cow Urine Distillate Co-administered with Levetiracetam in Epileptic Rats: A Pharmacokinetic and Pharmacodynamics Approach

Background: Epilepsy is a severe neurological condition that affects all ages of people. Complex pathways involved in pathogenesis make it complicated to treat; selected antiepileptic drug options are available for Epilepsy. There is a need for an hour to develop novel treatment approaches for epilepsy with lesser side effects. This research aimed to evaluate the alleviating role of bio-enhancers co-administered with levetiracetam for pilocarpine-induced epilepsy. Methodology: Pilocarpine (250 mg/kg) was used to develop epilepsy in rats. Levetiracetam (LEV) (140 mg/kg) was administered with Zingiber officinale Extract (ZOE) (15 mg/kg and 30 mg/kg) and Cow Urine Distillate (CUD) (1.5 ml/kg and 3 ml/kg). HPLC was used to evaluate drug concentration in blood. Serum nitrate, catalase, CRP, calcium level and calcium level of the brain, behavioural markers in rats were assessed and compared with the Leviteracetam group only. Result and Discussion: The present study showed that combining ZOE and CUD with levetiracetam was advantageous through substantial reduction (p &lt; 0.05) in serum nitrate, CRP and increased catalase (p &lt; 0.05), while reduced serum calcium compared to LEV alone. Combination of ZOE and CUD with levetiracetam treatment also reduced seizure behaviour and duration in rats. The bioavailability of LEV in plasma and brain was increased when epileptic rats were treated with LEV plus ZOE and CUD compared to disease control. Conclusion: Utilization of Zingiber officinale and CUD in combination with LEV was proven therapeutically effective in the epileptic model and used to lower the dose of LEV along with reducing seizure behaviour and time with the potential for the treatment of epilepsy.

Potential Benefits of Epidermal Growth Factor for Inhibiting Muscle Degrative Markers in Rats with Alcoholic Liver Damage.

This study investigated the beneficial effects of epidermal growth factor (EGF) on muscle loss in rats with chronic ethanol feeding. Six-week-old male Wistar rats were fed either a control liquid diet without EGF (C group, n = 12) or EGF (EGF-C group, n = 18) for two weeks. From the 3rd to 8th week, the C group was divided into two groups. One was continually fed with a control liquid diet (C group), and the other one was fed with an ethanol-containing liquid diet (E group); moreover, the EGF-C group was divided into three groups, such as the AEGF-C (continually fed with the same diet), PEGF-E (fed with the ethanol-containing liquid diet without EGF), and AEGF-E (fed with the ethanol-containing liquid diet with EGF). As a result, the E group had significantly higher plasma ALT and AST, endotoxin, ammonia, and interleukin 1b (IL-1b) levels, along with liver injuries, such as hepatic fatty changes and inflammatory cell infiltration. However, plasma endotoxin and IL-1b levels were significantly decreased in the PEGF-E and AEGF-E groups. In addition, the protein level of muscular myostatin and the mRNA levels of forkhead box transcription factors (FOXO), muscle RING-finger protein-1 (MURF-1) and atorgin-1 was increased considerably in the E group but inhibited in the PEGF-E and AEGF-E groups. According to the principal coordinate analysis findings, the gut microbiota composition differed between the control and ethanol liquid diet groups. In conclusion, although there was no noticeable improvement in muscle loss, EGF supplementation inhibited muscular protein degradation in rats fed with an ethanol-containing liquid diet for six weeks. The mechanisms might be related to endotoxin translocation inhibition, microbiota composition alteration as well as the amelioration of liver injury. However, the reproducibility of the results must be confirmed in future studies.

Jasminum humile (Linn) ameliorates CCl4-induced oxidative stress by regulating ER stress, inflammatory, and fibrosis markers in rats.

Jasminum humile (Linn) is highly valued for its medicinal properties. The pulp and decoction made from its leaves are effective for skin diseases. Juice prepared from roots is used against ringworm illness. Our current study aims to illustrate the non-toxicity and protective potential of methanol extract of Jasminum humile (JHM) against CCl4-induced oxidative stress in the liver of rats. Qualitative phytochemical screening, total flavonoids (TFC), and total phenolic content (TPC) assays were performed with JHM. The toxicity of the plant was estimated by treating female rats at different JHM doses while to assess anti-inflammatory potential of plant nine groups of male rats (six rats/group) received different treatments such as: CCl4 only (1ml/kg mixed with olive oil in a ratio of 3:7), silymarin (200mg/kg) + CCl4, different doses of JHM alone at a ratio of 1:2:4, and JHM (at a ratio of 1:2:4) + CCl4, and were examined for different antioxidant enzymes, serum markers, and histological changes, while mRNA expression of stress, inflammatory and fibrosis markers were assessed by real-time polymerase chain reaction analysis. Different phytochemicals were found in JHM. A high amount of total phenolic and flavonoid content was found (89.71 ± 2.79mg RE/g and 124.77 ± 2.41mg GAE/g) in the methanolic extract of the plant. Non-toxicity of JHM was revealed even at higher doses of JHM. Normal levels of serum markers in blood serum and antioxidant enzymes in tissue homogenates were found after co-administration of JHM along with CCl4. However, CCl4 treatment caused oxidative stress in the liver by enhancing the levels of stress and inflammatory markers and reducing antioxidant enzyme levels, while JHM treatment showed significant (P < 0.05) downregulation was in mRNA expression of those markers. Investigation of mechanism of specific signaling pathways related to apoptosis and clinical trials to assess safety and efficacy of optimal dosage of Jasminum humile will be helpful to develop FDA-approved drug.

Endoplasmic Reticulum Stress-Activated Neuronal and Microglial Autophagy Contributes to Postoperative Cognitive Dysfunction in Neonatal rats.

Surgery and anesthesia in neonates may lead to cognitive impairment or abnormal behaviors. It has been shown that autophagy plays a critical role in neuropsychiatric disorders, while the role of autophagy in postoperative cognitive impairment in neonates is not known. Here, we determined this role and the involvement of endoplasmic reticulum (ER) stress in regulating brain cell autophagy after surgery. Seven-day old neonatal rats (P7) had right common carotid artery exposure under anesthesia with 3% sevoflurane for 2h. Learning and memory were tested using Barnes maze (BM) and fear conditioning (FC) on P31-42 and P42-44, respectively. In another experiment, rat brains were harvested for biochemical studies. The ratio of microtubule-associated protein 1 light chain 3 (LC3) BII/I was increased and sequestosome 1 (P62/SQSTM1) levels were decreased in the brain 24h after surgery and anesthesia in neonatal rats. Immunofluorescent staining of LC3B was co-localized with a neuronal or a microglial marker but was not co-localized with a marker for astrocytes in rats with surgery. These rats had a poorer performance in the BM and FC tests than control rats when they were adolescent. Pretreatment with an autophagy inhibitor, 3-methyladenine, attenuated the poor performance. Surgery and anesthesia increased the expression of 78kDa glucose-regulated protein (BIP/GRP78), an indicator of ER stress, 6h after surgery and anesthesia. The ER stress activator tunicamycin and inhibitor tauroursodeoxycholic acid increased the markers for autophagy in control rats and decreased the autophagy markers in rats with surgery, respectively. Our results suggest that surgery in neonatal rats induces ER stress that then activates neuronal and microglial autophagy, which contributes to learning and memory impairment later in life.

Impact of a modified implant macrogeometry on biomechanical parameters and bone-related markers in rats.

This study investigated the impact of a modified implant macrogeometry on peri-implant healing and its effect on bone-related molecules in rats. Eighteen rats received one implant in each tibia: the control group received implants with conventional macrogeometry and the test group received implants with modified macrogeometry. After 30 days, the implants were removed for biomechanical analysis and the bone tissue around them was collected for quantifying gene expression of OPN, Runx2, β-catenin, BMP-2, Dkk1, and RANKL/OPG. Calcein and tetracycline fluorescent markers were used for analyzing newly formed bone at undecalcified sections of the tibial implants. These fluorescent markers showed continuous bone formation at cortical bone width and sparse new bone formed along the medullary implant surface in both groups. However, higher counter-torque values and upregulation of OPN expression were achieved by test implants when compared to controls. The modified macrogeometry of implants optimized peri-implant healing, favoring the modulation of OPN expression in the osseous tissue around the implants.

Avaliação do limiar nociceptivo e marcadores inflamatórios em ratos após indução de enfisema pulmonar por elastase nos modelos de dor fásica, inflamatória e neuropática

Avaliação do limiar nociceptivo e marcadores inflamatórios em ratos após indução de enfisema pulmonar por elastase nos modelos de dor fásica, inflamatória e neuropática

Evaluation of the nociceptive threshold and inflammatory markers in rats after induction of pulmonary emphysema by elastase in the phasic, inflammatory and neuropathic pain models

Evaluation of the nociceptive threshold and inflammatory markers in rats after induction of pulmonary emphysema by elastase in the phasic, inflammatory and neuropathic pain models

Fiber-like Action of d-Fagomine on the Gut Microbiota and Body Weight of Healthy Rats.

The goal of this work is to explore if the changes induced by d-fagomine in the gut microbiota are compatible with its effect on body weight and inflammation markers in rats. Methods: Sprague Dawley rats were fed a standard diet supplemented with d-fagomine (or not, for comparison) for 6 months. The variables measured were body weight, plasma mediators of inflammation (hydroxyeicosatetraenoic acids, leukotriene B4, and IL-6), and the concentration of acetic acid in feces and plasma. The composition and diversities of microbiota in cecal content and feces were estimated using 16S rRNA metabarcoding and high-throughput sequencing. We found that after just 6 weeks of intake d-fagomine significantly reduced body weight gain, increased the plasma acetate concentration, and reduced the plasma concentration of the pro-inflammatory biomarkers' leukotriene B4, interleukin 6 and 12 hydroxyeicosatetraenoic acids. These changes were associated with a significantly increased prevalence of Bacteroides and Prevotella feces and increased Bacteroides, Prevotella, Clostridium, and Dysgonomonas while reducing Anaerofilum, Blautia, and Oribacterium in cecal content. In conclusion, d-fagomine induced changes in the composition and diversity of gut microbiota similar to those elicited by dietary fiber and compatible with its anti-inflammatory and body-weight-reducing effects.

Europinidin Inhibits Rotenone-Activated Parkinson's Disease in Rodents by Decreasing Lipid Peroxidation and Inflammatory Cytokines Pathways.

Background: Europinidin is a derivative of delphinidin obtained from the plants Plumbago Europea and Ceratostigma plumbaginoides. This herb has wide medicinal applications in treating various diseases but there are very few studies available on this bioactive compound. Considering this background, the present study is designed for the evaluation of Europinidin against Parkinson’s disease. Aim: The investigation aims to assess the effect of Europinidin in the rotenone-activated Parkinson’s paradigm. Methods: To evaluate neuroprotective activity, rotenone (1.5 mg/kg s.c) and europinidin (10 mg/kg and 20 mg/kg) was administered in rats for 21 days. The behavioural parameters were performed before sacrificing the rats. On the 22nd day, all the rats were assessed for biochemical markers (SOD, GSH, MDA, Catalase), neurotransmitter levels (Dopamine, 5-HIAA, DOPAC, and HVA levels), and neuroinflammatory markers (IL-6, IL-1β and TNF-α). Results: It was found that rotenone produced significant (p < 0.001) oxidative damage, a cholinergic deficit, dopaminergic loss, and a rise in neuroinflammatory markers in rats. Conclusion: The study concludes that europinidin possesses anti-oxidant and anti-inflammatory properties. The results suggest the therapeutic role of europinidin against rotenone-activated behavioural, biochemical, and neuroinflammatory alterations in rats.

Epigenomics of rats' liver and its cross-species functional annotation reveals key regulatory genes underlying short term heat-stress response

Molecular responses to heat stress are multifaceted and under a complex cellular post-transcriptional control. This study explores the epigenetic and transcriptional alterations induced by heat stress (42 °C for 120 min) in the liver of rats, by integrating ATAC-seq, RNA-Seq, and WGBS information. Out of 2586 differential ATAC-seq peaks induced by heat stress, 36 up-regulated and 22 down-regulated transcript factors (TFs) are predicted, such as Cebpα, Foxa2, Foxo4, Nfya and Sp3. Furthermore, 150,189 differentially methylated regions represent 2571 differentially expressed genes (DEGs). By integrating all data, 45 DEGs are concluded as potential heat stress response markers in rats. To comprehensively annotate and narrow down predicted markers, they are integrated with GWAS results of heat stress parameters in cows, and PheWAS data in humans. Besides better understanding of heat stress responses in mammals, INSR, MAPK8, RHPN2 and BTBD7 are proposed as candidate markers for heat stress in mammals.

Effect of High-Intensity Interval Training on Cardiac Apoptosis Markers in Methamphetamine-Dependent Rats.

Chronic methamphetamine use increases apoptosis, leading to heart failure and sudden cardiac death. Previous studies have shown the importance of high-intensity interval training (HIIT) in reducing indices of cardiac tissue apoptosis in different patients, but in the field of sports science, the molecular mechanisms of apoptosis in methamphetamine-dependent rats are still unclear. The present article aimed to investigate the changes in cardiac apoptosis markers in methamphetamine-dependent rats in response to HIIT. Left ventricular tissue was used to evaluate caspase-3, melusin, FAK, and IQGAP1 gene expression. Rats were divided into four groups: sham, methamphetamine (METH), METH-control, and METH-HIIT. METH was injected for 21 days and then the METH-HIIT group performed HIIT for 8 weeks at 5 sessions per week. The METH groups showed increased caspase-3 gene expression and decreased melusin, FAK, and IQGAP1 when compared to the sham group. METH-HIIT showed decreased caspase-3 and increased melusin and FAK gene expression compared with the METH and METH-control groups. The IQGAP1 gene was higher in METH-HIIT when compared with METH, while no difference was observed between METH-HIIT and METH-control. Twenty-one days of METH exposure increased apoptosis markers in rat cardiac tissue; however, HIIT might have a protective effect, as shown by the apoptosis markers.

Effects of Dietary Gingerol-Enriched Ginger Supplementation on Distribution of Colon Function Markers in Rats With Diabetic Neuropathic Pain

ObjectivesInflammation and leaky gut may contribute to the pathogenesis of diabetic neuropathic pain (DNP). Ginger has been used in the treatment of a variety of pain disorders for its anti-inflammatory, antioxidant, and analgesic effects. We previously reported that gingerol-enriched ginger (GEG) supplementation suppressed the DNP-induced mRNA expression levels of claudin-3 (tight junction protein), PINK1 (autophagy marker), DRP1 (mitochondrial fission protein), and GFAP (astrocyte marker) in colons. Thus, this study was to further investigate the effects of GEG supplementation on the distribution of function markers in the colon of DNP rats. MethodsMale Sprague-Dawley rats were assigned to three groups: low-fat diet (Control), high-fat diet (HFD)+ streptozotocin (DNP), and HFD + streptozotocin + 0.75% GEG w/w in diet (DNP + GEG). Colons were collected and preserved at -80 degrees. The localization and quantity of claudin-3, PINK1, DRP1, and GFAP in colons were determined by cryosectioning, immunohistochemistry and fluorescence confocal microscopy. The protein levels were quantified by the average fluorescence intensity in cross-sections of intestinal crypts within pre-determined regions of interest (ROIs), normalized by the background ROI. The comparisons between groups were made using an unpaired t-test. ResultsCompared to the Control group, the DNP group had higher expression levels of claudin-3 (Control, n = 6; DNP, n = 5; P < 0.005), PINK1 (Control, n = 7; DNP, n = 7; P < 0.05), and DRP1 (Control, n = 6; DNP, n = 7; P < 0.01) in colons of animals. GEG supplementation into diets significantly suppressed DNP-induced expression levels of claudin-3 (DNP, n = 7, DNP + GEG, N = 6; P < 0.05), PINK1 (DNP, n = 7, DNP + GEG, n = 5; P < 0.05), and DRP1 (DNP, n = 7, DNP + GEG, n = 6; P < 0.05) in colons of animals. There were no significant differences in PINK1 expression between the Control group and the DNP + GEG group (p > 0.05). Similar to PINK1 finding, we did not observe the difference in DRP1 expression between the Control and the DNP + GEG group. ConclusionsThese findings show that gingerol-enriched ginger reduces the physiological colonic disruption associated with diabetic neuropathy. Funding SourcesMedical Student Summer Research Program, Texas Tech University Health Sciences Center, Lubbock, TX.

Protective effects of the ethanolic fenugreek seeds extract and its potentiation with nitric oxide modulators in adjuvant induced changes in arthritic index, proinflammatory/anti-inflammatory cytokines imbalance and oxidative stress markers in rats

Objectives: The current study was designed to evaluate protective role of the ethanolic fenugreek seed extract (FSE) and potentiating its effects with nitric oxide (NO) modulators in experimental arthritis and its comparison with the standard drug methotrexate. Materials and Methods: The FSE was prepared using standard procedures. Fifty-four male Wistar rats were equally distributed into nine groups of six animals in each group. Rheumatoid arthritis was induced by administration of complete Freund’s adjuvant (CFA) in sub-plantar region of rt. hind paw. FSE alone and with L-arginine or Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) were administered on day 10 of CFA inoculation, i.p. Animals were evaluated for arthritic parameters, cytokines and oxidative stress markers estimation. Statistics: The data were analysed by two-way ANOVA followed by Newman Keul’s post hoc test for inter group analysis by GraphPad Prism 6.0 and P &lt; 0.05 was taken as significant. Results: Adjuvant inoculated rat shows significant increase in arthritic and inflammatory parameters as well as oxidative stress biomarkers in serum, paw homogenates and joint synovial fluid. CFA inoculation significantly decreased anti-inflammatory cytokine-10 and SOD activity. These adjuvant-induced arthritic changes were significantly attenuated by ethanolic FSE administration from 10 to 28 days. These results are comparable to standard drug methotrexate. NO modulators further potentiated protective effects of FSE when given in combination. These results were more prominent when ethanolic seed extract was given with iNOS inhibitor, L-NAME. Conclusion: These findings suggest that FSE shows protective effects in CFA induced arthritic changes that may be mediated through pro-inflammatory/anti-inflammatory cytokines imbalance and it is associated with modulation of oxidative stress and NO-signalling.

Benzo[a]pyrene exposure in muscle triggers sarcopenia through aryl hydrocarbon receptor-mediated reactive oxygen species production

BackgroundBenzo[a]pyrene (BaP), a toxic carcinogen, is associated with various adverse effects but is rarely discussed in muscle-related disorders. This study investigated in vitro and in vivo effects triggered by BaP exposure in muscles and hypothesized that exposure might induce conditions similar to sarcopenia due to the shared mechanism of oxidative stress. In vitro experiments used C2C12 mouse myoblasts to examine effects induced by BaP exposure in control (untreated) and BaP-treated (10 µM/ml) muscle cells. An established TNF-α-treated sarcopenia model was utilized to verify our results. In vivo experiments compared immunohistochemical staining of sarcopenia-related markers in rats exposed to clean air and polluted air. ResultsIn C2C12 cells, after 2–72 h of BaP exposure, elevated mRNA and protein expressions were observed in aryl hydrocarbon receptor (AhR) and cytochrome P450 1A1, subsequently in ROS (NOX2 and NOX4) production, inflammatory cytokines (IL-6, TNF-α, and NF-kB), and proteins mediating apoptotic cell death (caspase-3 and PARP). Two myokines also altered mRNA and protein expressions akin to changes in sarcopenia, namely decreased irisin levels and increased myostatin levels. In addition, N-acetylcysteine, a well-known antioxidant, led to decrease in oxidative markers induced by BaP. The validation by TNF-α-treated sarcopenia model revealed comparable biological responses in either TNF-α or BaP treated C2C12 cells. In vivo experiments with rats exposed to air pollution showed increased expression of BaP, AhR, 8-hydroxydeoxyguanosine, and myostatin and decreased irisin expression in immunohistochemical staining. ConclusionsOur results suggest that BaP exerts deleterious effects on the muscle, leading to conditions indicative of sarcopenia. Antioxidant supplementation may be a treatment option for BaP-induced sarcopenia, but further validation studies are needed.

Lupeol inhibits pesticides induced hepatotoxicity via reducing oxidative stress and inflammatory markers in rats

The present study was aimed at investigating the toxicity of various pesticides on rat liver. It also aimed to show whether this toxicity could be avoided using lupeol. Adult male Wistars albino rats were randomly divided into nine groups. Control groups were given saline, corn oil, and lupeol; pesticide groups were given malathion, chlorpyrifos, and tebuconazole; in the other three treatments, same doses of pesticides and lupeol were given to the rats for ten days. Histopathological examination showed severe degenerative changes in the pesticide groups. Serum AChE activities, liver GSH, total antioxidant capacity levels, AChE, CAT, SOD, GPx, GR, Na+/K+-ATPase, ARE, and PON were decreased, while serum TNF-α, liver LPO, HP, NO, AOPP, total oxidant status, ROS, and oxidative stress index levels as well as AST, ALT, ALP, GST, arginase and xanthine oxidase activities were increased in the pesticides administered groups. It was observed that the PCNA levels determined by the immunohistochemical method increased in the pesticide groups. Also, the results Raman spectroscopy suggest that the technique may be used to understand/have an insight into pesticide toxicity mechanisms. The administration of lupeol demonstrated a hepatoprotective effect against pesticide-induced toxicity.

Arrested Acetylene-Induced Pulmonary and Testicular Toxicity in Rats Through Treatment With Polyphenols

Occupational exposure to potentially harmful substances is one of the dangers associated with industrial jobs. This study evaluated the modulatory influence of selected dietary polyphenols on the pulmonotoxic and testiculotoxic effects of crude acetylene, an industrial gas used in welding metals. Wistar rats were exposed to 58 000 ppm acetylene, 20 min daily for 30 days, in a 36 L glass inhalation chamber. Some acetylene-exposed animals were treated concurrently with 30 mg/kg quercetin, rutin, caffeic acid, ferulic acid, or coumaric acid. At the end of the treatment sessions, the levels of superoxide dismutase, reduced glutathione, glutathione peroxidase, lactate dehydrogenase, and hormonal markers in rats exposed to acetylene were significantly decreased, with a concomitant increase in lipid peroxidation, nitric oxide level, cholesterol concentration, and histopathological abnormalities. These damaging biochemical and histopathological changes were significantly ameliorated in animals administered the polyphenols. Quercetin showed greater ameliorative activity than rutin while the phenolic acids exhibited increasing levels of ameliorative activity in the order: caffeic acid > ferulic acid > coumaric acid. These results indicate that inhalation of crude acetylene is deleterious to the lungs and testes, and polyphenols provide protection against these detrimental effects.

Microbial Composition of a Traditional Fermented Wheat Preparation—Nishasta and Its Role in the Amelioration of Retinoic Acid-Induced Osteoporosis in Rats

Fermented foods have a long history of human use. The purpose of this study was to characterize the microbial composition of a traditional fermented wheat preparation—Nishasta— and to explore its effect in retinoic acid-induced osteoporosis in Wistar rats. The sample was suspended in sterile water (10% w/v), mixed thoroughly, filtered, and gradually diluted. Aliquots of dilutions were cultured in MRS (DeMan–Rogosa–Sharpe) medium, and colonies with similar morphologies were subjected to DNA extraction. The 16S rRNA gene of the isolates was amplified by polymerase chain reaction, checked by agarose gel electrophoresis, and finally identified by sequencing. Anti-osteoporosis screening of Nishasta was carried out in female Wistar rats using retinoic acid as an inducer (70 mg/kg, p.o. once a day for 14 days). Its effect on bone health parameters was determined. The bone metabolism markers such as hydroxyproline (HOP), tartrate-resistant acid phosphatase (TRACP), and alkaline phosphatase (ALP) were evaluated. The results of microbial characterization revealed the presence of ten clones of Lactobacillus plantarum in the fermented preparation with L. plantarum NF3 as the predominant strain. The average microbial count was 2.4 × 103 CFU/g. Retinoic acid administration led to a marked disorder of various bone health markers in rats. It also increased the levels of urine calcium and phosphorus, indicating increased bone destruction. Treatment with fermented wheat (at 200, 100, and 50 mg/kg doses, p.o. daily for 42 days after the induction of osteoporosis) improved bone mineral density in a dose-dependent manner. It also improved the bone microstructure and reduced the levels of ALP, TRACP, and HOP. Micro-CT revealed that it reduced trabecular separation and increased the percent bone volume, trabecular numbers, trabecular thickness, and bone mineral density in the rats. The results showed that the fermented wheat promoted bone formation and prevented bone resorption. Our findings clearly established the effectiveness of Nishasta against osteoporosis in Wistar rats that can be partly attributed to the improved gut calcium absorption and microbiota composition.