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Beetroot ( Beta vulgaris L.) is globally recognized for its outstanding color and flavor. It has been acknowledged for its therapeutic value since the ancient Romans. It is used to treat cardiovascular disorders. The therapeutic benefits of red beetroot are due to the substantial amounts of various bioactive metabolites, such as ascorbic acid, carotenoids, nitrates, phenolics, and betalains. However, the bioavailability and shelf life of these substances are significantly affected by the considerable variations in their processing methods among different countries. The longevity of the extracts is prolonged by employing well-established preservation techniques, such as boiling and steaming, which involve the application of heat. Our study aimed to analyze and compare the phytochemical composition of raw and heat processed beetroot using UPLC-QTOF-MS/MS. In addition, the study aimed to assess the effectiveness of processed beetroot in protecting against cardiovascular complications in a rat model of obesity induced by high-fat diet (HFD). UPLC-QTOF-MS/MS phytochemical profiling revealed the presence of 51 compounds, including organic acids, flavonoids, phenolics, betanins, and saponins. All the extracts demonstrated a significant decline in MDA, TNF- α , and IL-6 levels, suppressed the TGF- β expression, and restored the serum catalase level to normal. Among all the tested extracts, the steamed extract exhibited the slightest percentage change in body weight (10.2 ± 6.4) and effectively lowered the TNF-α level to normal levels. In contrast, the normal histological structure of heart muscle fibers was notably preserved in the cardiac sections of rats pretreated with steamed and boiled beetroot extracts. Additionally, mild caspase-3 immunoreactivity was observed in the cardiac muscles. The current study demonstrated that the steamed beetroot extract showed improved cardioprotective properties compared to the fresh and boiled extracts.

Hexavalent chromium salt, like potassium dichromate (PD), is chromium’s most precarious valence state in industrial wastes. Recently, there has been increasing interest in β-sitosterol (BSS), a bioactive phytosterol, as a dietary supplement. BSS is recommended in treating cardiovascular disorders due to its antioxidant effect. Trimetazidine (TMZ) was used traditionally for cardioprotection. Through the administration of BSS and TMZ, the cardiotoxic effects of PD were to be countered in this study, in addition to examining the precise mechanism of PD-induced cardiotoxicity. Thirty male albino rats were divided into five groups; the control group: administered normal saline daily (3 mL/kg); the PD group: administered normal saline daily (3 mL/kg); BSS group: administered BSS daily (20 mg/kg); TMZ group: administered TMZ daily (15 mg/kg); and the BSS + TMZ group: administered both BSS (20 mg/kg) and TMZ (15 mg/kg) daily. All experimental groups, except the control, received on the 19th day a single dose of PD (30 mg/kg/day, S.C.). Normal saline, BSS, and TMZ were received daily for 21 consecutive days p.o. The exposure to PD promoted different oxidative stresses, pro-inflammatory, and cardiotoxicity biomarkers. BSS or TMZ succeeded solely in reducing these deleterious effects; however, their combination notably returned measured biomarkers close to normal values. The histopathological investigations have supported the biochemical findings. The combination of BSS and TMZ protects against PD cardiotoxicity in rats by reducing oxidative stress and apoptotic and inflammatory biomarkers. It may be promising for alleviating and protecting against PD-induced cardiotoxicity in people at an early stage; however, these findings need further clinical studies to be confirmed. Highlights • Potassium dichromate induces cardiotoxicity in rats through the upregulation of oxidative stress, proinflammatory, and apoptotic pathways biomarkers. • β-Sitosterol possesses a possible cardioprotective effect by modulating several signaling pathways. • Trimetazidine, the antianginal agent, has a potential cardioprotective impact on PD-intoxicated rat model. • The combination of β-Sitosterol and trimetazidine was the best in modulating different pathways involved in PD cardiotoxicity in rats via the interplay between NF-κB/AMPK/mTOR/TLR4 and HO-1/NADPH signaling pathways. Graphical Abstract

Liver fibrosis, marked by excessive extracellular matrix deposition and chronic inflammation, is a significant health concern that can progress to cirrhosis and liver failure. Current treatments are limited, highlighting the need for novel therapies. Nicorandil (NIC), a potassium channel opener with nitric oxide-donating properties, has shown cytoprotective and anti-inflammatory effects. This study evaluates the efficacy of NIC in attenuating thioacetamide (TAA)-induced liver fibrosis in rats, focusing on the AMPK/SIRT-1/HIF-1α signaling pathway. Twenty-four adult male albino rats were randomly assigned to four groups: a control group, a TAA-treated group, and two groups treated with NIC at doses of 7.5 mg/kg/day and 15 mg/kg/day, respectively, for six weeks. TAA was administered intraperitoneally for six weeks to induce fibrosis, while NIC was given concurrently at both doses. TAA administration caused marked liver injury and fibrosis, as shown by increased ALT, AST, collagen-1α, and hydroxyproline levels. NIC treatment, particularly at 15 mg, significantly reduced these markers, indicating improved liver function and less fibrosis. NIC also alleviated oxidative stress by increasing SOD and GSH while lowering MDA, NO₂⁻, and iNOS. At the molecular level, NIC upregulated AMPK, SIRT-1, P53, and PGC-1α, and downregulated HIF-1α and STAT3. It further suppressed pro-inflammatory cytokines (IL-6, IL-1β, TNF-α, NF-κB, TGF-β1) while elevating IL-10. Histopathology confirmed improved liver structure with reduced collagen deposition, and immunohistochemistry showed decreased COX-II expression. In conclusion, both NIC doses showed therapeutic potential, with the 15 mg dose demonstrating superior efficacy. These findings highlight NIC’s promise as an effective treatment for liver fibrosis by mediating the AMPK/SIRT-1/HIF-1α pathway and modulating key molecular and cellular processes.

In this study, the anti-inflammatory effects of the methanolic extract (TE) of Plumeria obtusa L. (aerial parts) and its fractions were evaluated in vitro, and active fraction was evaluated in vivo. Among tested extracts, dichloromethane fraction (DCM-F) exhibited the strongest inhibition of lipopolysaccharide (LPS)-induced nitric oxide (NO) in RAW 264.7 macrophages. The effect of DCM-F on LPS-induced acute lung injury (ALI) in mice was studied. The animals were divided into five groups ( n  = 7) randomly; Gp I: negative control, GP II: positive control (LPS group), GP III: standard (dexamethasone, 2 mg/kg b.wt), GP IV and V: DCM-F (100 mg/kg), and DEM-F (200 mg/kg), respectively. DCM-F at a dose of 200 mg/kg suppressed the ability of LPS to increase the levels of nitric oxide synthase (iNOS), NO, tumor necrosis factor-α (TNF-α), and interleukin 6 (IL-6), as measured by ELISA. In addition, the expression of cyclooxygenase-2 (COX-2) was reduced (determined by immunohistochemistry) and the level of malondialdehyde (MDA) was decreased while that of catalase was restored to the normal values. Furthermore, the histopathological scores of inflammation induced by LPS were reduced. Twenty-two compounds were tentatively identified in DCM-F using LC/ESI-QToF with iridoids, phenolic derivatives and flavonoids as major constituents. Identified compounds were subjected to two different molecular docking processes against iNOS and prostaglandin E synthase-1 target receptors. Notably, protoplumericin A and 13- O -coumaroyl plumeride were the most promising members compared to the co-crystallized inhibitor in each case. These findings suggested that DCM-F attenuates the LPS-induced ALI in experimental animals through its anti-inflammatory and antioxidant potential.

Background Sodium butyrate (SB) is a short-chain fatty acid and a safe antibiotic alternative. During 35 days, this study compared the impact of coated SB (Butirex C4) and lincomycin (Lincomix) on broiler growth, gut health, and litter hygiene in 1200 one-day-old Ross-308 broiler chicks that were randomly assigned into 5-dietary groups with 5-replications each. Groups divided as follows: T1: Basal diet (control), T2: Basal diet with buffered SB (1 kg/ton starter feed, 0.5 kg/ton grower-finisher feeds), T3: Basal diet with 100 g/ton lincomycin, T4: Basal diet with buffered SB (0.5 kg/ton starter feed, 0.25 kg/ton grower-finisher feeds) + 50 g/ton lincomycin, and T5: Basal diet with buffered SB (1 kg/ton starter feed, 0.5 kg/ton grower-finisher feeds) + 50 g/ton lincomycin. Birds were housed in a semi-closed deep litter house, where feed and water were available ad libitum. Results were statistically analyzed using ANOVA and Tukey’s post hoc tests. Results Combined dietary supplementation with SB and lincomycin (T4 and T5) significantly enhanced body weights, weight gains, feed conversion ratio, and profitability index. Also, carcasses in T4 and T5 exhibited the highest dressing, breast, thigh, and liver yields. T5 revealed the best blood biochemical indices, while T3 showed significantly elevated liver and kidney function indices. T4 and T5 exhibited the highest expression levels of IGF-1 and TLR4 genes, the greatest villi length of the intestinal mucosa, and the lowest levels of litter moisture and nitrogen. Clostridia perfringens type A alpha-toxin gene was confirmed in birds’ caeca, with the lowest clostridial counts defined in T4. Conclusions Replacing half the dose of lincomycin (50 g/ton) with 0.5 or 1 kg/ton coated SB as a dietary supplement mixture showed the most efficient privileges concerning birds’ performance and health.

Background Recently, silver nanoparticles (Ag-NPs) were shown to provoke oxidative stress through the release of reactive oxygen species and consequently induce cell damage. Selenium-loaded chitosan nanoparticles (CS-SeNPs) have anti-inflammatory and antioxidant effects, indicating that they ameliorate Ag-NPs-induced ovarian toxicity. Objective This study aimed to assess how well CS-SeNPs counteract the damaging effects of Ag-NPs on the ovarian tissue of adult female albino rats. Methods Forty mature female albino rats were divided into four equal groups: for 60 days, Group I (control) was given 0.5 ml/kg of distilled water; Group II was given Ag-NPs orally (100 mg/kg); Group III was given Ag-NPs orally (100 mg/kg/d) plus CS-SeNPs (0.5 mg/kg/d); and Group IV was given only CS-SeNPs orally (0.5 mg/kg/d). All the ovarian tissues were removed and underwent immunohistochemical, histological, and biochemical analyses. Results Ag-NPs-exposed rats revealed a marked reduction in reduced glutathione (GSH) and superoxide dismutase (SOD). Numerous histopathological alterations were found along with a significant increase in PCNA- and Caspase-3-immunoreactive cells. Most of these alterations were successfully ameliorated by CS-SeNPs, as indicated by marked increases in GSH and SOD. Conclusion CS-SeNPs ameliorate the toxic effects of Ag-NPs on the ovarian tissue of adult female albino rats.

Acute lung injury (ALI) is a life-threatening condition usually associated with poor therapeutic outcomes and a high mortality rate. Since 2019, the situation has worsened due to the COVID-19 pandemic. ALI had approximately 40% of deaths before COVID-19, mainly due to the dysfunction of the blood–gas barrier that led to lung edema, failure of gas exchange, and dyspnea. Many strategies have been taken to mitigate the disease condition, such as diuretics, surfactants, antioxidants, glucocorticoids, heparin, and ventilators with concomitant sedatives. However, until now, there is no available effective therapy for ALI. Thus, we are presenting a new compound termed Arabincoside B (AR-B), recently isolated from Caralluma arabica, to be tested in such conditions. For that, the lipopolysaccharide (LPS) mice model was used to investigate the capability of the AR-B compound to control the ALI compared to standard dexamethasone. The results showed that AR-B had a significant effect on retrieving ALI. A further mechanistic study carried out in the serum, lung homogenate, histological, and immunohistochemistry sections revealed that the AR-B either in 50 mg/kg or 75 mg/kg dose inhibited pro-inflammatory cytokines such as IL-6, IL-13, NF-κB, TNFα, and NO and stimulated regulatory cytokines IL-10. Moreover, AR-B showed a considerable potential to protect the pulmonary tissue against oxidative stress by decreasing MDA and increasing catalase and Nrf2. Also, the AR-B exhibited an anti-apoptotic effect on the lung epithelium, confirmed by reducing COX and BAX expression and upregulating Bcl-2 expression. These results pave its clinical application for ALI.

This study aimed to synthesize zinc oxide nanoparticles (ZnO-NPs) via a green sustainable approach using Raphanus sativus (L.) root extract and evaluate their gastroprotective effect against ethanol-induced gastric injury in rats. ZnO-NPs were characterized through UV–Vis spectroscopy, FT-IR, TEM, zeta potential analysis, and XRD. LC- MS-coupled metabolic profiling was employed to identify different phytochemical compounds in the plant. Oxidative stress biomarkers (GSSG, GPX, and CAT), gastric secretions (gastrin and histamine), inflammatory cytokines (TNF-α and NF-κB), and molecular markers (MMP-10 and pERK1/2) were evaluated. Treatment with ZnO-NPs and plant extract restored antioxidant enzyme activity in a dose-dependent manner and decreased oxidative and inflammatory markers. Histopathological and histochemical analyses confirmed the protection of the gastric mucosa. The ZnO-NPs at (200 mg/kg), showed superior efficacy over the extract and, in some cases, displayed equivalent or enhanced effects relative to the reference drug omeprazole. In silico findings support the gastroprotective potential of the plant by demonstrating strong binding associations for major phytochemicals. This paper highlights that green-synthesized ZnO-NPs exhibit a significant gastroprotective effect through the modulation of oxidative stress and inflammatory pathways, indicating their promise as a safe and effective alternative treatment for gastric ulcers.

Plants belonging to the Launaea genus have been extensively utilized ethnopharmacologically to treat a variety of diseases, including kidney disorders. Chromium is a common industrial pollutant that has been linked to kidney disease. The present work was designed for the investigation of the UPLC-QTOF–MS/MS metabolite profile of the L. mucronate ethanolic extract (LME), along with assessing the mechanistic protective actions of LME and its nano-silver formulation (LMNS) against K2Cr2O7-induced nephrotoxicity in rats. LMNE was successfully biosynthesized and confirmed using UV–Visible (UV–Vis) spectroscopy and transmission electron microscopy (TEM). The nephroprotective effects of LME and LMNE was assessed in rats exposed to potassium dichromate (K2Cr2O7, 15 mg/kg BW) to cause nephrotoxicity. LME and LMNS, separately, were administered twice daily for 14 days at doses of 200 and 400 mg/kg BW, respectively. The kidney function, catalase, UGT, Nrf2, PGE2, Cox-2, ERK, and MAPK levels in renal tissue were all assessed, along with histopathological examinations for exploring their ameliorative effects. Forty-five bioactive metabolites were annotated belonging to flavonoids, phenolic and organic acids, coumarins, and fatty acids. Metabolite profiling revealed that chlorogenic acid, apigenin, and luteolin glycosides were the main phenolics, with chlorogenic acid-O-hexoside reported for the first time in LME. The findings revealed that the serum kidney function indicators (urea and creatinine) were markedly elevated in K2Cr2O7-intoxicated rats. Furthermore, inflammatory indicators (COX-2 and PGE2), MAPK, and ERK were all markedly elevated in kidney tissue, whereas catalase, UGT, and Nrf2 levels were downregulated. Histological and immunohistochemical assays confirmed the toxic effects of K2Cr2O7 in the kidneys. In contrast, the administration of LME and LMNS prior to K2Cr2O7 considerably improved the architecture of the renal tissue, while also restoring levels of most biochemical markers. Functioning via the inhibition of the MAPK/ERK pathway, activating Nrf2, and modifying the antioxidant and metabolic enzymes, LME and LMNS exerted their nephroprotective effects against K2Cr2O7-induced toxicity.

Chemotherapeutic-related toxicity exacerbates the increasing death rate among cancer patients, necessitating greater efforts to find a speedy solution. An in vivo assessment of the protective effect of the C. macrocarpa leaves polar fraction of hydromethanolic extract against doxorubicin (Dox)-induced neurotoxicity was performed. Intriguingly, this fraction ameliorated Dox-induced cognitive dysfunction; reduced serum ROS and brain TNF-α levels, upregulated the brain nerve growth factor (NGF) levels, markedly reduced caspase-3 immunoexpression, and restored the histological architecture of the brain hippocampus. The in vivo study results were corroborated with a UPLC-ESI-MS/MS profiling that revealed the presence of a high percentage of the plant polyphenolics. Molecular modeling of several identified molecules in this fraction demonstrated a strong binding affinity of flavan-3-ol derivatives with TACE enzymes, in agreement with the experimental in vivo neuroprotective activity. In conclusion, the C. macrocarpa leaves polar fraction possesses neuroprotective activity that could have a promising role in ameliorating chemotherapeutic-induced side effects.