AIM: To determine the dose of monosodium iodoacetate (MIA) required to induce oxidative stress, as well as pain and edema; to confirm the induction of knee osteoarthritis (OA) symptoms in rats by the presence of reactive oxygen species (ROS) and reduction of antioxidant agents; and to verify the presence of histopathological injury in these affected joints. METHOD: Biological markers of oxidative stress, pain, knee edema, and cartilage degeneration provided by different doses of MIA (0.5; 1.0 or 1.5 mg) in rat knee joints were analyzed. The animal evaluations were conducted during 15 days for mechanical and cold hypersensitivity, spontaneous pain and edema. After that, blood serum, intra-articular lavage and structures of knee, spinal cord and brainstem were collected for biochemical analysis; moreover, the knees were removed for histological evaluation. RESULTS: This study demonstrates that the highest dose of MIA (1.5 mg) increased the oxidative stress markers and reduced the antioxidant reactions, both in the focus of the lesion and in distant sites. MIA also induced the inflammatory process, characterized by pain, edema, increase in neutrophil count and articular damage. CONCLUSION: This model provides a basis for the exploration of underlying mechanisms in OA and the identification of mechanisms that may guide therapy and the discovery of OA signals and symptoms.
AIM: To determine the dose of monosodium iodoacetate (MIA) required to induce oxidative stress, as well as pain and edema; to confirm the induction of knee osteoarthritis (OA) symptoms in rats by the presence of reactive oxygen species (ROS) and reduction of antioxidant agents; and to verify the presence of histopathological injury in these affected joints. METHOD: Biological markers of oxidative stress, pain, knee edema, and cartilage degeneration provided by different doses of MIA (0.5; 1.0 or 1.5 mg) in rat knee joints were analyzed. The animal evaluations were conducted during 15 days for mechanical and cold hypersensitivity, spontaneous pain and edema. After that, blood serum, intra-articular lavage and structures of knee, spinal cord and brainstem were collected for biochemical analysis; moreover, the knees were removed for histological evaluation. RESULTS: This study demonstrates that the highest dose of MIA (1.5 mg) increased the oxidative stress markers and reduced the antioxidant reactions, both in the focus of the lesion and in distant sites. MIA also induced the inflammatory process, characterized by pain, edema, increase in neutrophil count and articular damage. CONCLUSION: This model provides a basis for the exploration of underlying mechanisms in OA and the identification of mechanisms that may guide therapy and the discovery of OA signals and symptoms.
Authors: Marcus Vinícius Viégas Lima; Abner de Oliveira Freire; Emerson Lucas Frazão Sousa; André Alvares Marques Vale; Alberto Jorge Oliveira Lopes; Cleydlenne Costa Vasconcelos; Mônica Virginia Viégas Lima-Aragão; Humberto Oliveira Serra; Rosane Nassar Meireles Guerra Liberio; Ana Paula Silva de Azevedo Dos Santos; Gyl Eanes Barros Silva; Claúdia Quintino da Rocha; Fernando César Vilhena Moreira Lima; Maria do Socorro de Sousa Cartágenes; João Batista Santos Garcia Journal: Molecules Date: 2019-09-25 Impact factor: 4.411
Authors: Hadeer Mohamed Hamdalla; Rasha Rashad Ahmed; Sanaa Rida Galaly; Osama Mohamed Ahmed; Ibrahim A Naguib; Badrah S Alghamdi; Manal Abdul-Hamid Journal: Stem Cells Int Date: 2022-08-16 Impact factor: 5.131