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Polyethylene microplastics (PE-MPs) are of significant concern due to their widespread use, pervasive persistence in the environment that induce multiple organ damage especially in the liver. Poncirin (PON) is a naturally present flavone with conspicuous pharmacological properties. the current investigation was formulated to ascertain the palliative role of PON against PE-MPs-provoked hepatic dysfunction. Twenty-four male albino rats were randomly divided into four groups: control, PE-MPs-treated (1.5 mg/kg), PE-MPs + PON co-treated (1.5 mg/kg and 20 mg/kg), and PON-treated (20 mg/kg). PE-MPs inebriation markedly lowered the expressions of antioxidant genes and Nrf-2, besides escalating Keap-1 expression. It also decreased antioxidants i.e., glutathione (GSH), glutathione S-transferase (GST), catalase (CAT), glutathione peroxidase (GPx), heme oxygenase-1 (HO-1), superoxide dismutase (SOD), glutathione reductase (GSR) activities, while remarkably upsurged reactive oxygen species (ROS) along with malondialdehyde (MDA) contents. Additionally, a notable escalation was observed in the levels of hepatic serum markers i.e., alkaline phosphatase (ALP), alanine transaminase (ALT) and aspartate aminotransferase (AST). Furthermore, PE-MPs exposure increased the levels of inflammatory biomarkers, including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), nuclear factor kappa B (NF-kB), interleukin-1β (IL-1β) levels and cyclooxygenase-2 (COX-2) activities. PE-MPs intoxication augmented the expressions of Caspase-3 and Bax along with decreasing the expression of Bcl-2. Nevertheless, PON treatment notably abated PE-MPs prompted liver injuries owing to its hepatoprotective efficacy. Thus, it may be inferred that PON could be a potential therapeutic option for treating hepatic damage caused by PE-MPs. [ABSTRACT FROM AUTHOR]

Polystyrene microplastics (PSMPs) are noxious environmental pollutants that pose a significant threat to vital body organs including the lungs. Robinetin (ROB) is a flavonoid which demonstrates various pharmacological potentials. This trial was designed to assess the protective ability of ROB to avert PSMPs provoked pulmonary toxicity in rats. Twenty-four rats were divided into four groups i.e., control, PSMPs (0.1 mg/kg), PSMPs (0.1 mg/kg) + ROB (30 mg/kg) and ROB (30 mg/kg) only supplemented group. PSMPs exposure led to a notable reduction in the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GSR) as well as GSH contents while causing a pronounced elevation in the concentration of MDA and ROS. Furthermore, PSMPs significantly augmented the levels of myeloperoxidase (MPO), macrophages, neutrophils, and lymphocytes in BALF. Moreover, the levels of IL-1β, TNF-α, NF-κB, IL-6 and COX-2 activities were increased following the PSMPs exposure. Nonetheless PSMPs remarkably decreased Bcl-2 levels, coupled with an escalation in Caspase-9, Caspase-3 and Bax levels. Despite this, severe histological alterations were observed in lungs tissues after PSMPs provision. Nevertheless, ROB provision markedly protected the lungs via regulating aforementioned dysregulations. This investigation validated the shielding strength of ROB to counteract PSMPs caused pulmonary toxicity. [ABSTRACT FROM AUTHOR]

Arsenic is a lethal toxicant found ubiquitously in the ecosystem which adversely affects the body organs including the heart. Pachypodol (PCHP) is a natural flavone which exhibits substantial pharmacotherapeutic potentials. The rats (n = 24) were distributed into 4 different groups i.e., control, arsenic-intoxicated group (50 mg/kg), arsenic + PCHP-supplemented group (50 mg/kg + 10 mg/kg) & PCHP-treated (10 mg/kg) group. It was assessed that arsenic administration subsided catalase (CAT), glutathione reductase (GSR), superoxide dismutase (SOD), glutathione peroxidase (GPx), & glutathione S-transferases (GST) activities while augmenting the levels of reactive oxygen species (ROS) and malondialdehyde (MDA). Furthermore, arsenic exposure increased the levels of cardiac injury markers such as creatine phosphokinase (CPK), creatine kinase-MB (CK-MB), troponin I & lactate dehydrogenase (LDH). Besides, the levels of inflammatory markers nuclear factor kappa B (NF-κB), interleukin-1β (IL-1β), Tumor necrosis factor α (TNF-α), Interleukin 6 (IL-6) levels and cyclooxygenase 2 (COX-2) activity were increased following the arsenic exposure. Similarly, Caspase-3, Bax and Caspase-9 levels were upsurged whereas Bcl-2 level was reduced after arsenic intoxication. In addition, the histopathological assessment revealed a substantial cardiac tissues impairment in the arsenic exposed group. Nonetheless, PCHP supplementation substantially (p < 0.05) recovered the abovementioned arsenic −induced impairments owing to its anti-inflammatory, antioxidative and anti-apoptotic abilities. Therefore, the current research revealed that PCHP might be a promising ameliorative agent to cure arsenic instigated cardiac damages. [ABSTRACT FROM AUTHOR]

Doxorubicin (DOX) is a potent chemotherapeutic agent that is used in various sorts of malignancies. However, its uses are restricted owing to its deleterious effects on different organs including the liver. Cupressuflavone (CUP) is a plant-based flavonoid which is well known for its biological as well pharmacological potential. Our investigation aimed to evaluate the ameliorative potential of CUP against DOX provoked liver toxicity in rats. Twenty-four albino rats (Rattus norvegicus) were distributed into four distinct groups such as control, DOX (3 mg/kg), co- administrated DOX (3 mg/kg) + CUP (40 mg/kg) and CUP (40 mg/kg) only. DOX exposure reduced catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), Glutathione reductase (GSR), glutathione-S-transferase (GST) activities and glutathione (GSH) content while escalating the levels of reactive oxygen species (ROS) and malondialdehyde (MDA). Besides, the levels of ALT, AST and ALP were increased in response to DOX exposure. Furthermore, administration of DOX upregulated the levels of Interleukin-6 (IL-6), Nuclear factor kappa-B (NF-κB), Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and the activity of cyclooxygenase-2 (COX-2). The treatment of DOX reduced the levels of Bcl-2 while escalating the levels of Caspase-3, Caspase-9 and Bax. Similarly, DOX intoxication instigated various histopathological disruptions in hepatic tissues of rats. However, supplementation of CUP notably (p < 0.05) restored abovementioned hepatic dysregulations owing to its anti-oxidative, anti-inflammatory as well as anti-apoptotic potential. Our results manifested that CUP could be used as hepatoprotective agent againt DOX induced liver damage in rats. [ABSTRACT FROM AUTHOR]

Paraquat (PQ) an herbicide that is commonly used to remove undesirable grasses. However, PQ also causes cardiac damage through reactive oxygen species (ROS) production. Didymin (DYD) is a dietary flavone, present in citrus fruits and campanula. DYD displays multiple therapeutic activities i.e., anti-oxidant, hepatoprotective, neuroprotective and free radical salvaging. Therefore, the present study was planned to explore the ameliorative effect of DYD against PQ instigated cardiac damage. 24 rats were separated into 4 groups, control, PQ administered PQ + DYD co-administered orally and DYD only administered group. PQ intoxication significantly reduced anti-oxidants including (SOD, GST, GSH, CAT, GPx and GSR activities, while increasing malondialdehyde (MDA) and ROS levels. PQ intoxication escalated the level of cardiac injury marker i.e., creatine kinase myoglobin binding (CK-MB), troponin, creatinine phosphokinase (CPK) and lactate dehydrogenase (LDH). PQ also augmented inflammatory markers i.e., (TNF-α, IL-1β, NF-κB, IL-6 levels and COX-2 activity). Moreover, PQ intoxication escalated the apoptotic proteins levels (Bax, Caspase-3 and Caspase-9), while decreasing Bcl-2 level. PQ intoxication also prompted histomorphological anomalies in the heart of rats. Conversely, DYD therapy restored all the anomalies and structural abnormalities owing to its cardioprotective potentials. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a hazardous heavy metal that adversely affects the vital body organs particularly liver. Eriocitrin (ERCN) is a plant-based flavonoid that is well-known for its wide range of pharmacological potential. This research trial was aimed to determine the ameliorative potential of ERCN against Cd provoked hepatotoxicity in rats. Twenty-four rats (Rattus norvegicus) were apportioned into control, Cd treated (5 mg/kg), Cd (5 mg/kg) + ERCN (25 mg/kg) and only ERCN (25 mg/kg) administrated group. Expressions of Nrf2/Keap1 pathway and apoptotic markers were assessed through qRT-PCR. The levels of inflammatory and liver function markers were evaluated by using standard ELISA kits. Cd exposure reduced the expression of Nrf2 and anti-oxidant genes as well as the activity of catalase (CAT), glutathione reductase (GSR), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione S-transferase (GST) and glutathione (GSH) contents while escalating the expression of Keap1. Furthermore, Cd intoxication augmented malondialdehyde (MDA) and reactive oxygen species (ROS) levels in hepatic tissues. Exposure to Cd resulted in a notable elevation in the levels of alanine transaminase (ALT), alkaline phosphatase (ALP) and aspartate aminotransferase (AST). Cd administration upregulated nuclear factor-kappa B (NF-κB), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) levels as well as cyclooxygenase-2 (COX-2) activity. Furthermore, Cd administration upsurged Bax and Caspase-3 expression while reducing the expression of Bcl-2. Moreover, Cd intoxication disrupted the normal architecture of hepatic tissues. However, supplementation of ERCN significantly (p < 0.05) ameliorated the aforementioned disruptions induced by Cd intoxication. ERCN treatment remarkably ameliorated the hepatic tissues owing to its antioxidant, anti-inflammatory, and anti-apoptotic potentials. These findings underscore the therapeutic potential of ERCN to counteract the adverse effects of environmental pollutants on hepatic tissues. • Cadmium dysregulated Nrf2/keap1 pathway and activities of antioxidant enzymes. • Cadmium escalated levels of oxidative stress hepatic function markers. • Cadmium increased the levels inflammatory markers. • Cadmium instigated various hepatic histological alterations. • Eriocitrin protected hepatic tissues via regulating abovementioned damages. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a noxious and non-biodegradable heavy metal which instigates various organ toxicities such as cardiac injuries. Pinostrobin (PSB) is a potent dietary bioflavonoid, which shows various pharmacological potentials. The current research was designed to evaluate the ameliorative effects of PSB against Cd elicited cardiac dysfunction in rats. Twenty-four albino rats were apportioned into four equal groups viz. control, Cd (5 mg/kg), Cd (5 mg/kg) + PSB (40 mg/kg) and PSB (40 mg/kg) only treated group. It was observed that Cd intoxication reduced catalase (CAT), glutathione reductase (GSR), superoxide dismutase (SOD), glutathione peroxidase (GPx), activities and glutathione S-transferase (GST) contents while escalating the levels of reactive oxygen species (ROS), hydrogen peroxide (H 2 O 2) and malondialdehyde (MDA). Furthermore, Cd exposure escalated the levels of cardiac injury markers such as creatine phosphokinase (CPK), creatine kinase-myocardial band (CK-MB), troponin I and lactate dehydrogenase (LDH). Besides, the levels of inflammatory cytokines nuclear factor- κB (NF-κB), interleukin 1beta (IL-1ß), tumor necrosis factor- α (TNF-α), interleukin-6 (IL-6) levels and cyclooxygenase-2 (COX-2) activity were upregulated in Cd intoxicated group. Similarly, Caspase-3, Bax and Caspase-9 levels were augmented, and Bcl-2 levels were reduced after Cd administration. In addition, the histopathological examination revealed a notable cardiac tissue impairment in the Cd exposed group. Nonetheless, PSB treatment significantly (p < 0.05) recovered the abovementioned Cd-induced impairments. Therefore, the current study revealed that PSB might be a promising ameliorative agent to ameliorate Cd instigated cardiac damages. [ABSTRACT FROM AUTHOR]

Paraquat (PQ) is an effective herbicide however, due to its adverse effects on different organs including heart, it is considered as highly toxic to human beings. Kaempferide (KMF) is a plant-based flavonoid with conspicuous pharmacological properties. This experiment was executed to evaluate the palliative actions of KMF on PQ prompted cardiac toxicity in rats. Twenty-four rats were apportioned into 4 equal groups which were designated as control, toxicant (PQ treated), Co-treated (PQ + KMF) and KMF group. After 30 days of treatment, PQ intoxication resulted in a remarkable reduction in antioxidant enzymes activities which include, glutathione reductase (GSH), glutathione S-transferase (GST), catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and glutathione disulfide reductase (GSR), whereas an elevation was observed in reactive oxygen species (ROS), & malondialdehyde (MDA) as well as hydrogen peroxide (H 2 O 2) level. Furthermore, concentrations of cardiac injury markers, creatinine phosphokinase (CPK), creatine kinase-myoglobin binding (CK-MB), & lactate dehydrogenase (LDH), as well as troponin I were increased in response to PQ treatment. Moreover, inflammatory cytokines such as tumour necrosis factor alpha (TNF-α), nuclear factor-kappa B (NF-κB), and interleukin-6 (IL-6), interleukin-1 beta (lL-1β), and cyclooxygenase-2 (COX-2) levels were augmented in PQ intoxicated group. PQ exposure reduced the gene expression of cardiac anti-apoptotic markers (Bcl-2), but the gene expression of apoptotic marker (caspase-9, caspase-3 and Bax) was increased. Histopathological damages were also observed in toxicant (PQ) exposed group. However, the administration of KMF significantly palliated PQ induced aforementioned disruptions. In the light of these findings, it is concluded that KMF is a promising bioactive compound that may be used as a curative agent against PQ instigated cardiac damage due to its marvelous antioxidant, anti-apoptotic, anti-inflammatory as well as cardioprotective potential. [ABSTRACT FROM AUTHOR]