2 articles
Pulmonary tuberculosis remains a major cause of morbidity and mortality worldwide. According to data published by the World Health Organization in 2024, a total of 8.2 million people were newly diagnosed with TB in 2023, compared with 7.5 million in 2022, 7.1 million in 2019, and markedly higher than the 5.8 million and 6.4 million in 2020 and 2021, respectively.
The prospective study involved 59 participants before and after treatment: 11 women (18.6%) and 48 men (81.4%). The participants were divided into 2 groups: group L1 – patients with tuberculosis before treatment, and group L2 – patients with tuberculosis after treatment. Serum levels of nitric oxide, malondialdehyde, glutathione reductase, and total antioxidant activity were measured using a spectrophotometric method.
In the study, we demonstrated that nitric oxide and malondialdehyde serum concentrations were non-significantly higher in the L2 group compared with the L1 group. Glutathione reductase activity showed a significant decrease in antioxidant activity in the L2 group, indicating reduced antioxidant capacity. Total antioxidant activity showed a non-significant decrease in the L1 group compared with the L2 group.
The results of the research demonstrated that the administered anti-tuberculosis treatment increased nitric oxide and malondialdehyde levels, and reduced glutathione reductase and total antioxidant activity. This phenomenon indicates the persistence of oxidative stress even after treatment. The levels of nitric oxide, malondialdehyde, glutathione reductase, and total antioxidant activity in patients with pulmonary tuberculosis may serve as biomarkers for monitoring disease progression.
Nitric oxide (NO) is a gaseous molecule that is a biological mediator that carries out important regulation of physiological processes necessary for the functioning of tissues. We hypothesized that nonspecific inhibition of all isoforms of NOs would cause pancreatic damage and created a model of experimental pancreatitis based on NOs inhibition. Along with the study of the mechanisms of development of chronic pancreatitis, the search for medicines to treat and inhibit the progression of this disease continues.
To study the protective effect of glutargin on the pancreas of rats with chronic pancreatitis induced by a blocker of NOs.
The work was carried out on 21 laboratory white male Wistar rats weighing 180-230 g. Chronic pancreatitis was induced by intraperitoneal administration of the NOs blocker - N-nitro-L-arginine (L-NNA) (Sigma-Aldrich, USA) at a dose of 40 mg/kg of body weight. Rats in group I (n = 7) were injected with L-NNA for 12 days, rats in group II (n = 7) were injected intraperitoneally with glutargin 20 mg/kg, after 20 minutes they were injected with L-NNA - within 12 days. Rats of the control group (n = 7) were injected intraperitoneally with 0.9% NaCl solution. The rats were euthanized on the 45th day and biochemical and morphological studies were carried out.
After the introduction of the NOs blocker, deterioration of the general condition of the animals was determined, a sharp increase in the level of nitrites/nitrates to 80.22±19.91 μmol/l, control 32.61±4.55 μmol/l (р < 0.05); protein-bound hydroxyproline (PBH) to 215.21±22.01μmol/l, control 178.67±26.39 μmol/l, (p < 0.05); free hydroxyproline (FH) to 14.74±1.84 μmol/l, control 9.96±0.71 μmol/l, (p < 0.05); malondialdehyde (MDA) to 5.67±0.88 nmol/ml, control 3.62±0.13, (р < 0.05). Pronounced structural changes with stasis of formed blood elements in the vessels, focal accumulation of leukocytes in the parenchyma, dystrophy of acinar cells and fibrosis in the atrophy zone were determined in the pancreas of rats. Administration of glutargin contributed to the restoration of general behavioral reactions of rats, normalization of MDA – 4.81±0.15 nmol/ml, control 4.50±0.23, (p > 0.05); ceruloplasmin (CP) – 591.71±68.07 mg/ml, control – 663.25±34.05 mg/ml, (p > 0.05); PBH 183.62±5.98 μmol/l, control – 179.28±9.19 μmol/l, (p > 0.05); FH – 9.44±1.13 μmol/l, control – 9.96±0.71 μmol/l, (p > 0.05) and prevented the development of pronounced structural changes in the pancreas.
In chronic pancreatitis induced by a NOs blocker, glutargin can prevent chronic pancreatitis by normalizing collagen metabolism, inhibiting oxidative stress, and severity of pancreatic parenchymal damage.