Betanin ameliorates Lipopolysaccharide-induced acute lung injury in mice via inhibition of inflammatory response and oxidative stress

Background: Acute lung injury (ALI) is the most common form of inflammatory disease, which has higher morbidity and mortality rates worldwide. ALI is characterized by alterations in the lungs such as epithelial dysfunction, excessive inflammation, and lung edema. Objective: The current work was aimed to unveil the abrogative properties of betanin on the LPS-induced ALI in mice. Methodology: In an in vitro assay, betanin-treated RAW 264.7 cells viability was evaluated by MTT assay. The TNF-α, IL-1β, and IL-6 levels in the cell lysates were estimated using assay kits. In in vivo studies, the ALI was initiated in the BALB/c mice by exposing them to a 3-day intra-tracheal challenge of 5 mg/kg of LPS and then treated with betanin (25 and 50 mg/kg) for three days. Later, the BALF samples were obtained from the mice and used to estimate the inflammatory biomarkers using assay kits. The levels of MDA and the antioxidants SOD and GSH were also examined using commerical kits. The iNOS, COX-2, and PGE-2 expressions were estimated using kits, and finally the histopathological study was conducted on the lung tissues. Results: The outcomes of in vitro studies revealed that betanin appreciably improved the viability of LPS-exposed RAW 264.7 cells. The betanin effectively diminished the levels of IL-6, IL-1β, and TNF-α in LPS-induced RAW 264.7 cells. In in vivo studies, the findings demonstrated that betanin treatment diminished the lung/bodyweight, lung W/D weight, and protein level in the ALI mice. The inflammatory cell counts and inflammatory biomarkers such as COX-2, PGE2, and iNOS were substantially reduced by the betanin treatment in the ALI mice. Betanin treatment also increased the GSH and SOD and reduced the MDA in the ALI mice. The histopathological alterations in the lungs tissues of ALI mice were effectively ameliorated by the betanin. Conclusion: In summary, the findings apparently suggest that betanin effectively ameliorated the LPS-triggered ALI in mice through its beneficial properties. Therefore, in the future, it can be used as a new salutary candidate to manage the ALI in medical settings

Diabetes mellitus and diabetic foot ulcer: Etiology, biochemical and molecular based treatment strategies via gene and nanotherapy

Diabetes mellitus (DM) is a collection of metabolic and pathophysiological disorders manifested with high glucose levels in the blood due to the inability of β-pancreatic cells to secrete an adequate amount of insulin or insensitivity of insulin towards receptor to oxidize blood glucose. Nevertheless, the preceding definition is only applicable to people who do not have inherited or metabolic disorders. Suppose a person who has been diagnosed with Type 1 or Type 2DM sustains an injury and the treatment of the damage is complicated and prolonged. In that case, the injury is referred to as a diabetic foot ulcer (DFU). In the presence of many proliferating macrophages in the injury site for an extended period causes the damage to worsen and become a diabetic wound. In this review, the scientific information and therapeutic management of DM/DFU with nanomedicine, and other related data were collected (Web of Science and PubMed) from January 2000 to January 2022. Most of the articles revealed that standard drugs are usually prescribed along with hypoglycaemic medications. Conversely, such drugs stabilize the glucose transporters and homeostasis for a limited period, resulting in side effects such as kidney damage/failure, absorption/gastrointestinal problems, and hypoglycemic issues. In this paper, we review the current basic and clinical evidence about the potential of medicinal plants, gene therapy, chemical/green synthesized nanoparticles to improving the metabolic profile, and facilitating the DM and DFU associated complications. Preclinical studies also reported lower plasma glucose with molecular targets in DM and DFU. Research is underway to explore chemical/green synthesized nanoparticle-based medications to avoid such side effects. Hence, the present review is intended to address the current challenges, recently recognized factors responsible for DM and DFU, their pathophysiology, insulin receptors associated with DM, medications in trend, and related complications. © 2022TRU

Protective effects of harmine on Monosodium Iodoacetate-induced Osteoarthritis in rats: In vitro and in vivo studies

Background: Osteoarthritis (OA) is a painful and debilitating disease, which is characterized by joint pain, swelling, restricted movement, and joint stiffness. It affects more than millions of people worldwide. Objective: In this current work, we aimed to assess the beneficial roles of harmine on the monosodium iodoacetate (MI)-induced OA in rats. Methodology: The in vitro studies were carried out in the LPS-induced RAW 264.7 cells and administered with 5 and 10 µM of harmine. In in vivo studies, 2.5 mg of MI diluted in 10 ml of saline (9%) was injected into the knee joints of the experimental rats to induce OA. The 25 and 50 mg/kg of harmine was treated one week before the MI injection and continued for 25 days after induction. The paw volume and arthritis score was measured after the completion of treatments. The levels of inflammatory cytokines, PGE-2, and NO in both RAW 264.7 cells and OA-induced rats using the assay kits. The MDA and antioxidants (GSH, CAT, and SOD) levels were assessed using the assay kits. The knee joint tissues were analyzed by histopathological study. Results: The treatment with 5 and 10 µM of harmine effectively decreased the PGE-2 and NO levels in the LPS-exposed RAW 264.7 cells. The status of IL-6 and TNF-α also diminished by the harmine in the LPS-induced RAW 264.7 cells. The paw volume and arthritis score was decreased by the harmine treatment. The levels of PGE-2, IL-6, IL-1β, and TNF-α levels were depleted and IL-10 level was augmented by the harmine treatment in the OA-induced rats. The harmine are also suppressed the MDA and elevated the GSH, SOD, and CAT in the OA-induced rats. Further, the therapeutic roles of harmine also evidenced by the findings of the histopathological analysis. Conclusion: The current research suggests that harmine is effective in attenuating OA in rats and significantly decreasing the OA-related oxidative stress and inflammation responses. The harmine also reduced the inflammatory response in the LPS-induced RAW 264.7 cells, therefore, it may be a talented agent for treating OA

Effects of In Ovo Supplementation with Nanonutrition (L-Arginine Conjugated with Ag NPs) on Muscle Growth, Immune Response and Heat Shock Proteins at Different Chicken Embryonic Development Stages

The aim of the study was to analyze the in ovo injection of inorganic and organic synthesized silver nanoparticles (Ag NPs) using Brassica oleracea L. var. capitate F. rubra (BOL) conjugation with L-Arginine (L-Arg) on the immune, muscle growth, survivability and hatchability of broiler chickens. The conjugation of L-Arg (100 μg) with 1000 µg of Ag NPs synthesized by (BOL)-extract and L-Arg (100 μg) conjugated with 100 µg of Ag NPs inorganic synthesized were injected into fertile eggs at 8 d, 14 d and 18 d of incubation. Survival and hatching rate were significantly improved in the dose of L-Arg (100 μg) with 1000 µg (BOL-Ag NPs) and L-Arg (100 μg) with 100 µg (C-Ag NPs) on 14 d injection whereas it was decreased on 8 d or 18 d injection. Moreover, the protein expression of muscle development markers such as myogenin and myoD were significantly uprelated in 14 d of incubation whereas the heat shock proteins (HSPs), such as HSP-60 and HSP-70, were significantly upregulated in 18 d incubation. In addition, the liver function marker of serum glutamate oxaloacetate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT) were significantly decreased and the immunoglobulin (IgM) levels were increased in a 14 d incubation period in serum at the same concentration

Modulatory effect of linoleic and oleic acid on cell proliferation and lipid metabolism gene expressions in primary bovine satellite cells

This study was performed to elucidate the effects of linoleic acid (LA), oleic acid (OA) and their combination (LA + OA) on cell proliferation, apoptosis, necrosis, and the lipid metabolism related gene expression in bovine satellite cells (BSCs), isolated from bovine muscles. Cell viability was significantly increased with the OA and LA treatment. Furthermore, LA + OA enhanced cell proliferation in a dose-dependent manner (10 to 100 µM), whereas it lowered at 250 µM. In addition, a cell-cycle analysis showed that 100 µM of LA and OA markedly decreased the G0/G1 phase proportion (62.58% and 61.33%, respectively), compared to controls (68.02%), whereas the S-phase cells’ proportion was increased. The ratio of G2/M phase cells was not significantly different among the groups. Moreover, analyses with AO/EtBr staining showed that no apoptosis occurred. Necrosis were determined by flow cytometry using Annexin V-FITC/PI staining which revealed no early apoptosis in the cells pretreated with LA or OA, but occurred in the LA + OA group. We also analyzed the mRNA expression of lipid metabolizing genes such as peroxisome proliferator receptor alfa (PPARα), peroxisome proliferator receptor gamma (PPARγ), acyl-CoA oxidase (ACOX), lipoprotein lipase (LPL), carnitine palmitoyl transferase (CPT-1), and fatty-acid binding protein4 (FABP4), which were upregulated in LA or OA treated cells compared to the control group. In essence, LA and OA alone promote the cell proliferation without any apoptosis and necrosis, which might upregulate the lipid metabolism related gene expressions, and increase fatty-acid oxidation in the BSCs’ lipid metabolism

Anticancer and antimicrobial potential of zinc/sodium alginate/polyethylene glycol/d-pinitol nanocomposites against osteosarcoma MG-63 cells

The field of nanomedicine has attracted much interest and is now serving as the impetus for many revolutionary advances in the pharmaceutical industry