Treatment with Lycopodium clavatum 200dH Intensifies Kidney and Liver Injury in Mice Infected with Toxoplasma gondii

Pereira, Andréia Vieira; Góis, Marcelo Biondaro; Lera, Katiucha Rebeca Jennifer Lopes; Miranda-Sapla, Milena Menegazzo; Falkowski-Temporini, Gislane Janaina; Bezerril, Juliana Evangelista; Zanusso-Junior, Gerson; Ferraz, Fabiana Nabarro; Silva, Suelen Santos da; Aleixo, Denise Lessa; Conchon‐Costa, Ivete; Sant’Ana, Débora de Mello Gonçales; Costa, Idessânia Nazareth; Araújo, Silvana Márques de; Pavanelli, Wander Rogério

doi:10.1007/s00005-020-00567-5

Cited by 5 publications

(4 citation statements)

References 36 publications

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“…These functions may be associated with the diverse composition of secondary metabolites found in their spores [ 31 ], such as serratan triterpenoids [ 32 ]. Besides the impact on CD, the use of LC has also been evaluated in other conditions, such as in experimental Toxoplasma gondii infection [ 33 , 34 ], in vitro cytotoxic effect on colon cancer cells [ 35 , 36 ], and in a pilot study in humans with irritable bowel syndrome [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Treatments for Digestive Forms of Chagas Disease in Experimental Models: A Systematic Review

Neto

Guerra

Rodrigues

et al. 2022

Oxidative Medicine and Cellular Longevity

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Chagas disease is an anthropozoonosis caused by the protozoan Trypanosoma cruzi and is characterized as a neglected disease. It is currently endemic in 21 countries on the Latin American continent, including Bolivia, Argentina, and Paraguay. Unfortunately, there are no optimally effective treatments that can reduce the damage caused in the digestive form of the disease, such as the neuronal destruction of the myenteric plexus of both the esophagus and the colon. Therefore, the objective of this systematic review was to report the possible pharmacological neuroprotective agents that were tested in murine models of the digestive form of Chagas disease. Inclusion criteria are in vivo experimental studies that used different murine models for digestive forms of Chagas disease related to pharmacological interventions with neuroprotective potential, without year and language restriction. On the other hand, the exclusion criteria were studies that did not approach murine models with the digestive form of the disease or did not use neuroprotective treatments, among others. The search in the PubMed, Web of Science, Embase, and LILACS databases was performed on September 4, 2021. In addition, a manual search was performed using the references of the included articles. The risk of bias assessment of the studies was performed based on the SYRCLE tool guidelines, and the data from the selected articles are presented in this review as a narrative description and in tables. Eight articles were included, 4 of which addressed treatment with acetylsalicylic acid, 3 with cyclophosphamide, and 1 with Lycopodium clavatum 13c. In view of the results of the studies, most of them show neuroprotective activity of the treatments, with the potential to reduce the number of damaged neurons, as well as positive changes in the structure of these cells. However, more studies are needed to understand the mechanisms triggered by each drug, as well as their safety and immunogenicity. Systematic review registration is as follows: PROSPERO database (CRD42022289746).

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Section: Discussionmentioning

confidence: 99%

Neuroprotective Treatments for Digestive Forms of Chagas Disease in Experimental Models: A Systematic Review

Neto

Guerra

Rodrigues

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Significant relationships exist between the TGF-β expression and the degree of kidney fibrosis [125]. Pereira et al [126] used immunohistochemistry staining to examine TGF-β in the kidneys of mice infected with T. gondii. Increased immunoexpression of the cytokine was observed at 7, 15, 30, and 60 dpi compared with the control group of animals.…”

Section: Transforming Growth Factor β (Tgf-β)mentioning

confidence: 99%

Pathomechanisms in the Kidneys in Selected Protozoan Parasitic Infections

Kot

Łanocha-Arendarczyk

Ptak

et al. 2021

IJMS

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Leishmaniasis, malaria, toxoplasmosis, and acanthamoebiasis are protozoan parasitic infections. They remain important contributors to the development of kidney disease, which is associated with increased patients’ morbidity and mortality. Kidney injury mechanisms are not fully understood in protozoan parasitic diseases, bringing major difficulties to specific therapeutic interventions. The aim of this review is to present the biochemical and molecular mechanisms in kidneys infected with Leishmania spp., Plasmodium spp., Toxoplasma gondii, and Acanthamoeba spp. We present available mechanisms of an immune response, oxidative stress, apoptosis process, hypoxia, biomarkers of renal injury in the serum or urine, and the histopathological changes of kidneys infected with the selected parasites. Pathomechanisms of Leishmania spp. and Plasmodium spp. infections have been deeply investigated, while Toxoplasma gondii and Acanthamoeba spp. infections in the kidneys are not well known yet. Deeper knowledge of kidney involvement in leishmaniasis and malaria by presenting their mechanisms provides insight into how to create novel and effective treatments. Additionally, the presented work shows gaps in the pathophysiology of renal toxoplasmosis and acanthamoebiasis, which need further research.

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“…Transforming growth factor-β 1 (TGF-β1) is the primary mediator of glomerulosclerosis leading to renal interstitial fibrosis (Song et al, 2017). As a strong fibrogenic factor, TGF-β1 has increased expression in the case of chronic glomerulitis (Pereira et al, 2010). Besides, it transfers extracellular signals into the nucleus based on proteins of the Smad family to cooperate with the expressions of related genes, which directly promotes the synthesis of type I collagen (Col-1) and the progression of glomerular fibrosis.…”

Section: Introductionmentioning

confidence: 99%

Effects of bradykinin on proliferation, apoptosis, and cycle of glomerular mesangial cells via the TGF-β1/Smad signaling pathway

Ding

Wang

et al. 2021

Turk J Biol

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We aimed to assess the effects of bradykinin (BK) on the proliferation, apoptosis, and cycle of glomerular mesangial cells via the transforming growth factor-β 1 (TGF-β1)/Smad signaling pathway. Rat glomerular mesangial cells, HBZY-1, were divided into normal group (untreated), model group (5 ng/L TGF-β1), BK group (5 ng/L TGF-β1 + 1 ng/L BK), and inhibitor group [5 ng/L TGF-β1 + 1 ng/L LY2109761 (TGF-β1-specific inhibitor)]. The cell proliferation, cycle, apoptosis, expression of type I collagen (Col-1), and protein expressions of Col-1, TGF-β1, and phosphorylated Smad2 (p-Smad2) were detected by EdU labeling, flow cytometry, acridine orange/ethidium bromide (AO/EB) dual staining, immunofluorescence assay, and Western blotting, respectively. Compared with the normal group, the cell proliferation rate (P = 0.02) and protein expression levels of Col-1 (P = 0.02), TGF-β1 (P = 0.01), p-Smad2 (P = 0.02), and p-Smad7 (P = 0.00) in the model group significantly increased, and apoptosis rate (P = 0.01) significantly decreased. Compared with the model group, the BK and inhibitor groups significantly decreased in proliferation rate (P = 0.01) and protein expression levels of Col-1 (P = 0.01), TGF-β1 (P = 0.01), and p-Smad2 (P = 0.00). Also, they were significantly elevated in apoptosis rate (P = 0.02) and p-Smad7 protein expression (P = 0.02). BK regulates the proliferation, apoptosis, and the cycle of glomerular mesangial cells by inhibiting the TGF-β1/Smad signaling pathway.

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Treatment with Lycopodium clavatum 200dH Intensifies Kidney and Liver Injury in Mice Infected with Toxoplasma gondii

Cited by 5 publications

References 36 publications

Neuroprotective Treatments for Digestive Forms of Chagas Disease in Experimental Models: A Systematic Review

Neuroprotective Treatments for Digestive Forms of Chagas Disease in Experimental Models: A Systematic Review

Pathomechanisms in the Kidneys in Selected Protozoan Parasitic Infections

Effects of bradykinin on proliferation, apoptosis, and cycle of glomerular mesangial cells via the TGF-β1/Smad signaling pathway

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