Ameliorative role of catechin to combat against lindane instigated liver toxicity via modulating PI3K/PIP3/Akt, Nrf-2/Keap-1, NF-κB pathway and histological profile.

Lindane (LDN) is a well-known herbicidal drug that exerts deleterious impacts on vital body organs including the liver. Catechin (CTN) is a plant-based flavonoid that demonstrates various pharmacological abilities. This trial was executed to evaluate the ameliorative efficacy of CTN to combat LDN instigated hepatotoxicity in male albino rats (Rattus norvegicus). Thirty-two rats were categorized into four groups including control, LDN (30 mg/kg), LDN (30 mg/kg) + CTN (40 mg/kg) and CTN (40 mg/kg) alone treated group. It was observed that LDN dysregulated the expressions of PI3K/PIP3/Akt and Nrf-2/Keap-1 pathway. Moreover, the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), heme­oxygenase-1 (HO-1) and glutathione reductase (GSR) were subsided after LDN intoxication. Besides, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), ALT (Alanine aminotransferase), AST (Aspartate transaminase), Gamma-glutamyl transferase (GGT) and ALP (Alkaline phosphatase) were increased whereas reduced the levels of albumin and total proteins in response to LDN exposure. Additionally, LDN administration escalated the levels of Interleukin-6 (IL-6), Nuclear factor kappa-B (NF-κB), Interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), and the activity of cyclooxygenase-2 (COX-2). Furthermore, the gene expressions of Bcl-2-associated X protein (Bax) and Cysteinyl aspartate-acid proteases-3 (Caspase-3) were enhanced whereas the expression of B-cell lymphoma-2 (Bcl-2) was lowered following the LDN treatment. LDN instigated various histological impairments in hepatic tissues. Nonetheless, concurrent administration of CTN remarkably ameliorated liver impairments via regulating aforementioned disruptions owing to its antioxidant, anti-apoptotic and histo-protective potentials.

Black cardamom essential oil prevents Escherichia coli O157:H7 and Salmonella Typhimurium JSG 1748 biofilm formation through inhibition of quorum sensing.

This study aimed to investigate the chemical composition, using GC-MS, and anti-biofilm potential of black cardamom essential oil (BCEO) against biofilms of Escherichia coli O157:H7 and Salmonella Typhimurium JSG 1748 through inhibition of bacterial quorum sensing. GC-MS quantification demonstrated that BCEO contains 1,8-cineole (44.24%), α-terpinyl acetate (12.25%), nerolidol (6.03%), and sabinene (5.96%) as the major bioactive compounds. Antioxidant assays for BCEO revealed the total phenolic and flavonoid mean values were 1325.03 ± 7.69 mg GAE 100/g and 168.25 ± 5.26 mg CE/g, respectively. In regards to antimicrobial potential, Candida albicans was the most sensitive species compared to Streptococcus mutans, Staphylococcus aureus, Listeria monocytogenes, Bacillus cereus, and Salmonella Typhimurium with the following zones of inhibition; 14.4 ± 0.52, 13.2 ± 0.42, 11.2 ± 0.28, 11.0 ± 0.52, 8.2 ± 0.24 and 6.6 ± 0.18 mm in diameter, respectively. Biofilm inhibition by BCEO was concentration-dependent, when various concentrations of 0.03, 0.06, 0.12, 0.25 and 0.5% were applied, 33.67, 34.14, 38.66, 46.65 and 50.17% of Salmonella Typhimurium biofilm was inhibited, while 47.31, 54.15, 76.57, 83.36 and 84.63% of Escherichia coli biofilm formation was prevented. Chromobacterium violaceum ATCC 12,472 and its product violacein, was used as a microbial indicator for enhancement or inhibition of quorum sensing. Our data showed that 0.5% of BCEO inhibited violacein production without influencing the growth of Chromobacterium violaceum, while 1% of BCEO, caused 100% inhibtion of violacein production together with 30% inhibition of growth. This study shows that BCEO possesses promising antioxidant and antimicrobial potential, and found anti-biofilm activities linked to the quenching of the quorum sensing system of E. coli and S. Typhimurium.

Pharmacotherapeutic potential of malvidin to cure imidacloprid induced hepatotoxicity via regulating PI3K/AKT, Nrf-2/Keap-1 and NF-κB pathway.

Imidacloprid (IMI) is one of the top-notch insecticides that adversely affects the body organs including the liver. Malvidin (MAL) is a natural flavonoid which exhibits a wide range of pharmacological properties. This research was designed to evaluate the protective ability of MAL to counteract IMI instigated liver toxicity in rats. Thirty-two rats were divided into four groups including control, IMI (5mg/kg), IMI (5mg/kg) + MAL (10mg/kg) and MAL (10mg/kg) alone treated group. The recommended dosages were administrated through oral gavage for 4 weeks. It was revealed that IMI intoxication disrupted the PI3K/AKT and Nrf-2/Keap-1 pathway. Furthermore, the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), heme-oxygenase-1 (OH-1) and glutathione reductase (GSR) were reduced while upregulating reactive oxygen species (ROS) and malondialdehyde (MDA) levels after IMI treatment. Moreover, IMI poisoning increased the levels of ALT (Alanine aminotransferase), AST (Aspartate transaminase), and ALP (Alkaline phosphatase) while reducing the levels of total proteins and albumin in hepatic tissues of rats. Besides, IMI administration escalated the expressions of Bcl-2-associated protein x (Bax) and cysteine-aspartic acid protease-3 (Caspase-3) while downregulating the expressions of B-cell lymphoma 2 (Bcl-2). Similarly, IMI intoxication, increased the levels of Interleukin-6 (IL-6), Nuclear factor kappa-B (NF-κB), Interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), and the activity of cyclooxygenase-2 (COX-2). Furthermore, IMI disrupted the normal architecture of hepatic tissues. However, MAL treatment remarkably protected the liver tissues via regulating abovementioned disruptions.