
The Potential of Nano Curcumin in Preventing the Formation of Artificial Antisperm Antibody in Wistar Rats through Inflammatory Pathway Regulation
Author(s) -
Didit Pramudhito,
Suwandi Sugandi,
Ida Parwati,
Muchtan Sujatno,
Soetojo Soetojo
Publication year - 2021
Publication title -
open access macedonian journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.288
H-Index - 17
ISSN - 1857-9655
DOI - 10.3889/oamjms.2021.5749
Subject(s) - curcumin , medicine , tumor necrosis factor alpha , dexamethasone , inflammation , cytokine , antibody , interleukin , pharmacology , immunology
BACKGROUND: Immunological mechanisms of infertility are still poorly understood and controversial, both the cause and treatment. Inflammation, immunology, cell proliferation, cell differentiation, and cell survival are influenced by several proteins, including nuclear factor kappa-B (NFĸB), tumor necrosis factor-α (TNF-α), and interleukin-10 (IL-10).
AIM: This study aimed to explore the potential of nano curcumin to prevent anti-sperm antibodies (ASA) formation due to the testes’ inflammatory process in Wistar rats.
METHODS: This research is an experimental study with a pre-post-test approach with control group. The research subjects were rats (Rattus norvegicus) of the Wistar strain. The induced animals were grouped into three groups: Group 1 received nano curcumin 1 × 80 mg/kg BW orally, Group 2 received dexamethasone 1 × 0.3 mg/kg BW, and Group 3 received placebo aquadest 1 × 1 mL orally. TNF-α, NF-kB, and IL10 levels in serum were examined with enzyme-linked immunosorbent assay.
RESULTS: The nano curcumin treatment showed the ability to reduce the pro-inflammatory cytokine protein TNF-α expression (47.3 ± 2.32) more optimally than dexamethasone treatment (54.4 ± 3.22). Nano curcumin has also shown the ability to reduce the pro-inflammatory cytokine transcription factor, NF-kB (32.5 ± 2.76) more optimally than treatment with dexamethasone (44.6 ± 2.43).
CONCLUSION: Nano curcumin can prevent the formation of ASA in testicular trauma through inhibition of the inflammatory response.