S-Methylcysteine (SMC) Ameliorates Intestinal, Hepatic, and Splenic Damage Induced by Cryptosporidium parvum Infection Via Targeting Inflammatory Modulators and Oxidative Stress in Swiss Albino Mice
Metadatos
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MDPI
Materia
Cryptosporidium parvum Hepatic damage Inflammatory biomarkers Intestinal injury s-Methylcysteine
Fecha
2020Referencia bibliográfica
Elmahallawy EK, Elshopakey GE, Saleh AA, Agil A, El-Morsey A, EL-shewehy DMM, Sad AS, Yanai T, Abdo W. S-Methylcysteine (SMC) Ameliorates Intestinal, Hepatic, and Splenic Damage Induced by Cryptosporidium parvum Infection Via Targeting Inflammatory Modulators and Oxidative Stress in Swiss Albino Mice. Biomedicines. 2020; 8(10):423.[https://doi.org/10.3390/biomedicines8100423]
Resumen
Cryptosporidiosis has been proposed to be one of the major causes of diarrhoeal disease in
humans worldwide that possesses zoonotic concern. Thereby, this study investigated the potential
effects of s-Methylcysteine (SMC) on the parasite in vivo followed by the measurement of cytokines,
oxidative stress parameters, and an investigation of the major histopathological changes. Sixty male
Swiss albino mice weighing 20–25 g were allocated equally into five groups and orally administered
saline only (control), SMC only (SMC50) (50 mg/kg b.w.), and 104 Cryptosporidium parvum oocysts
per mouse via an esophageal tube (C + ve untreated). The fourth and fifth groups (C + SMC25,
C + SMC50) administrated 104 C. parvum oocysts combined with SMC25 (low dose) and 50 (high
dose) mg/kg b.w., respectively. At days 7 and 14 post-infection (PI), the feces was collected from
each group in order to count C. parvum oocysts. After two weeks of treatment, the animals were
euthanized and the serum was collected for biochemical analysis. Next, the intestinal, spleen, and
liver sections were dissected for histopathological examination. The results revealed lower oocyst
numbers in the C + SMC25 and C + SMC50 groups compared to the infected untreated group.
Moreover, higher doses of SMC treatment significantly reduced the enteritis induced by C. parvum in a
dose-dependent manner. The hepatic lesions were also mitigated as demonstrated in C + SMC25 and C + SMC50 groups unlike the infected group via lowering the serum alanine aminotransferase (ALT),
aspartate aminotransferase (AST), and alkaline phosphatase (ALP) enzymes and increasing albumin
and globulin serum levels. SMC administration also reduced cytokines production (SAP, TNF-α, IL-6,
and IFN-γ) mediated by Cryptosporidium infection in contrast to the infected untreated group. There
were marked lymphoid depletion and amyloidosis observed in the infected untreated group, while
the treated groups showed obvious increase in the lymphoid elements. Moreover, the scoring of
intestinal parasites, hepatic, and splenic lesions in the SMC-treated groups exhibited significantly
lower pathological lesions in different organs in a dose-dependent manner, compared to the infected
untreated group. Our results also revealed a significant change in the malondialdehyde content with
an elevation of glutathione and superoxide dismutase in the intestines collected from C + SMC25
and C + SMC50 mice relative to the untreated group. Taken together, our results indicated that
SMC could be a promising effective compound for treating and declining C. parvum infestation via
restoring structural alterations in different tissues, enhancing antioxidant enzymes, and suppressing
the cytokines liberation.