Abstract:Cisplatin is widely used as one of the most effective anticancer agents in the treatment of some neoplasms. Reproductive toxicity is the most common outcome associated with cisplatin testicular damage. Alternative natural medicines for treating male testicular disorders and infertility have received extensive attention in research. Natural products, medicinal herbs, and their secondary metabolites have been shown as promising agents in the management of testicular damage induced by chemotherapy drugs. This stu… Show more
“…Cisplatin can induce the production of reactive oxygen species (ROS) and reduce the activity of antioxidant enzymes, leading to oxidative stress and damage to testicular cells [ 1 ]. In addition, cisplatin can activate the Nuclear factor kappa-B (NF-κB) signaling pathway and increase the expression of pro-inflammatory cytokines, leading to inflammation and tissue damage [ 19 ]. Furthermore, cisplatin can directly damage DNA and induce apoptosis in testicular cells [ 15 ].…”
Section: Discussionmentioning
confidence: 99%
“…In addition, cisplatin can activate the Nuclear factor kappa-B (NF-κB) signaling pathway and increase the expression of pro-inflammatory cytokines, leading to inflammation and tissue damage [19]. Furthermore, cisplatin can directly damage DNA and induce apoptosis in testicular cells [15].…”
In recent years, adipose-derived stem cells (ADSCs) and derived exosomes (ADSC-Ex) have been investigated for their therapeutic potential in various diseases due to their satisfactory differentiation and regeneration ability. We aimed to explore the potential treatment of ADSCs and ADSC-Ex for testicular injury caused by cisplatin. ADSCs and ADSC-Ex s were identified and extracted to treat the rat model with testicular injury caused by cisplatin. Then the immunohistochemistry and Enzyme linked immunosorbent assay (ELISA) were used to detect the potential treatment of ADSCs and ADSC-Ex. We found that ADSCs and ADSC-Ex significantly improved the testicular tissue damage, increased the number of germ cells, and improved the arrangement of the seminiferous tubules. The levels of malondialdehyde and testosterone were also improved. We speculated that ADSCs and ADSC-Ex may alleviate the testicular injury caused by cisplatin.
“…Cisplatin can induce the production of reactive oxygen species (ROS) and reduce the activity of antioxidant enzymes, leading to oxidative stress and damage to testicular cells [ 1 ]. In addition, cisplatin can activate the Nuclear factor kappa-B (NF-κB) signaling pathway and increase the expression of pro-inflammatory cytokines, leading to inflammation and tissue damage [ 19 ]. Furthermore, cisplatin can directly damage DNA and induce apoptosis in testicular cells [ 15 ].…”
Section: Discussionmentioning
confidence: 99%
“…In addition, cisplatin can activate the Nuclear factor kappa-B (NF-κB) signaling pathway and increase the expression of pro-inflammatory cytokines, leading to inflammation and tissue damage [19]. Furthermore, cisplatin can directly damage DNA and induce apoptosis in testicular cells [15].…”
In recent years, adipose-derived stem cells (ADSCs) and derived exosomes (ADSC-Ex) have been investigated for their therapeutic potential in various diseases due to their satisfactory differentiation and regeneration ability. We aimed to explore the potential treatment of ADSCs and ADSC-Ex for testicular injury caused by cisplatin. ADSCs and ADSC-Ex s were identified and extracted to treat the rat model with testicular injury caused by cisplatin. Then the immunohistochemistry and Enzyme linked immunosorbent assay (ELISA) were used to detect the potential treatment of ADSCs and ADSC-Ex. We found that ADSCs and ADSC-Ex significantly improved the testicular tissue damage, increased the number of germ cells, and improved the arrangement of the seminiferous tubules. The levels of malondialdehyde and testosterone were also improved. We speculated that ADSCs and ADSC-Ex may alleviate the testicular injury caused by cisplatin.
“…Such is the case of cisplatin, which causes mainly nephrotoxic damage, with over 30% of patients presenting acute and chronic renal lesions [59]. Moreover, cisplatin could induce neurotoxicity, hepatotoxicity, ototoxicity, and testicular damage [60][61][62][63].…”
Colorectal cancer (CRC) is the third most common neoplasia in the world. Its mortality rate is high due to the lack of specific and effective treatments, metastasis, and resistance to chemotherapy, among other factors. The natural products in cancer are a primary source of bioactive molecules. In this research, we evaluated the antitumor activity of an acetogenin (ACG), laherradurin (LH), isolated from the Mexican medicinal plant Annona macroprophyllata Donn.Sm. in a CRC murine model. The CRC was induced by azoxymethane–dextran sulfate sodium (AOM/DSS) in Balb/c mice and treated for 21 days with LH or cisplatin. This study shows for the first time the antitumor activity of LH in an AOM/DSS CRC model. The acetogenin diminished the number and size of tumors compared with cisplatin; the histologic studies revealed a recovery of the colon tissue, and the blood toxicity data pointed to less damage in animals treated with LH. The TUNEL assay indicated cell death by apoptosis, and the in vitro studies exhibited that LH inhibited cell migration in HCT116 cells. Our study provides strong evidence of a possible anticancer agent for CRC.
Mitochondria are the “gatekeeper” in a wide range of cellular functions, signaling events, cell homeostasis, proliferation, and apoptosis. Consequently, mitochondrial injury is linked to systemic effects compromising multi-organ functionality. Although mitochondrial stress is common for many pathomechanisms, individual outcomes differ significantly comprising a spectrum of associated pathologies and their severity grade. Consequently, a highly ambitious task in the paradigm shift from reactive to predictive, preventive, and personalized medicine (PPPM/3PM) is to distinguish between individual disease predisposition and progression under circumstances, resulting in compromised mitochondrial health followed by mitigating measures tailored to the individualized patient profile. For the successful implementation of PPPM concepts, robust parameters are essential to quantify mitochondrial health sustainability. The current article analyses added value of Mitochondrial Health Index (MHI) and Bioenergetic Health Index (BHI) as potential systems to quantify mitochondrial health relevant for the disease development and its severity grade. Based on the pathomechanisms related to the compromised mitochondrial health and in the context of primary, secondary, and tertiary care, a broad spectrum of conditions can significantly benefit from robust quantification systems using MHI/BHI as a prototype to be further improved. Following health conditions can benefit from that: planned pregnancies (improved outcomes for mother and offspring health), suboptimal health conditions with reversible health damage, suboptimal life-style patterns and metabolic syndrome(s) predisposition, multi-factorial stress conditions, genotoxic environment, ischemic stroke of unclear aetiology, phenotypic predisposition to aggressive cancer subtypes, pathologies associated with premature aging and neuro/degeneration, acute infectious diseases such as COVID-19 pandemics, among others.
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