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Article ; Online: Inflammatory response to Trichomonas vaginalis in the pathogenesis of prostatitis and benign prostatic hyperplasia.

Han, Ik-Hwan / Kim, Jung-Hyun / Ryu, Jae-Sook

Parasites, hosts and diseases

2023 Volume 61, Issue 1, Page(s) 2–14

Abstract: Trichomonas vaginalis is a flagellated protozoan that causes trichomoniasis, a common nonviral sexually transmitted infection. T. vaginalis infection is asymptomatic in most infected men but can lead to chronic infection. The inflammatory response to ... ...

Abstract	Trichomonas vaginalis is a flagellated protozoan that causes trichomoniasis, a common nonviral sexually transmitted infection. T. vaginalis infection is asymptomatic in most infected men but can lead to chronic infection. The inflammatory response to chronic T. vaginalis infection may contribute to prostatic diseases, such as prostatitis and benign prostatic hyperplasia (BPH); however, studies on the relationship between T. vaginalis infection and prostate diseases are scarce. In this review, we discuss evidence from our studies on the involvement of T. vaginalis in the pathogenesis of prostate diseases, such as prostatitis and BPH. Studies of prostatitis have demonstrated that the attachment of T. vaginalis trophozoite to prostate epithelial cells (PECs) induces inflammatory cytokine production and inflammatory cell migration, leading to prostatitis. T. vaginalis also causes pathological changes, such as inflammatory cell infiltration, acinar changes, interstitial fibrosis, and mast cell infiltration, in prostate tissues of infected rats. Thus, T. vaginalis is considered an infectious agent that triggers prostatitis. Meanwhile, studies of prostatic hyperplasia revealed that mast cells activated by T. vaginalis-infected prostate cells secreted inflammatory mediators, such as β-hexosaminidase and tryptase, which promoted proliferation of prostate stromal cell (PSC). Moreover, interleukin-6 produced by proliferating PSCs induced the multiplication of BPH-1 epithelial cells as a result of stromal-epithelial interaction, suggesting that the proliferation of T. vaginalis-infected prostate cells can be induced through crosstalk with mast cells. These collective findings suggest that T. vaginalis contributes to the progression of prostatitis and prostatic hyperplasia by creating an inflammatory microenvironment involving PECs and PSCs.
MeSH term(s)	Male ; Humans ; Rats ; Animals ; Trichomonas vaginalis/physiology ; Prostatitis/pathology ; Prostatic Hyperplasia/pathology ; Trichomonas Infections/complications ; Prostate
Language	English
Publishing date	2023-02-22
Publishing country	Korea (South)
Document type	Review ; Journal Article
ISSN	2982-6799
ISSN (online)	2982-6799
DOI	10.3347/PHD.22160
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: The involvement of the noradrenergic system in the antinociceptive effect of cucurbitacin D on mice with paclitaxel-induced neuropathic pain.

Park, Keun-Tae / Kim, Suyong / Choi, Ilseob / Han, Ik-Hwan / Bae, Hyunsu / Kim, Woojin

Frontiers in pharmacology

2023 Volume 13, Page(s) 1055264

Abstract: Paclitaxel (sold under the brand name Taxol) is a chemotherapeutic drug that is widely used to treat cancer. However, it can also induce peripheral neuropathy, which limits its use. Although several drugs are used to attenuate neuropathy, no optimal ... ...

Abstract	Paclitaxel (sold under the brand name Taxol) is a chemotherapeutic drug that is widely used to treat cancer. However, it can also induce peripheral neuropathy, which limits its use. Although several drugs are used to attenuate neuropathy, no optimal treatment is available to date. In this study, the effect of cucurbitacins B and D on paclitaxel-induced neuropathic pain was assessed. Multiple paclitaxel injections (a cumulative dose of 8 mg/kg, i. p.) induced cold and mechanical allodynia from days 10 to 21 in mice, and the i. p. administration of 0.025 mg/kg of cucurbitacins B and D attenuated both allodynia types. However, as cucurbitacin B showed a more toxic effect on non-cancerous (RAW 264.7) cells, further experiments were conducted with cucurbitacin D. The cucurbitacin D dose-dependently (0.025, 0.1, and 0.5 mg/kg) attenuated both allodynia types. In the spinal cord, paclitaxel injection increased the gene expression of noradrenergic (
Language	English
Publishing date	2023-01-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2022.1055264
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Article ; Online: Enhanced Therapeutic Effect of Optimized Melittin-dKLA, a Peptide Agent Targeting M2-like Tumor-Associated Macrophages in Triple-Negative Breast Cancer.

Kim, Soyoung / Choi, Ilseob / Han, Ik-Hwan / Bae, Hyunsu

International journal of molecular sciences

2022 Volume 23, Issue 24

Abstract: Triple-negative breast cancer (TNBC) is characterized by a high possibility of metastasis. M2-like tumor-associated macrophages (TAMs) are the main components of the tumor microenvironment (TME) and play a key role in TNBC metastasis. Therefore, TAMs may ...

Abstract	Triple-negative breast cancer (TNBC) is characterized by a high possibility of metastasis. M2-like tumor-associated macrophages (TAMs) are the main components of the tumor microenvironment (TME) and play a key role in TNBC metastasis. Therefore, TAMs may be a potential target for reducing TNBC metastasis. Melittin-dKLA, a peptide composed of fused melittin and pro-apoptotic peptide d(KLAKLAK)2 (dKLA), showed a potent therapeutic effect against cancers by depleting TAMs. However, melittin has a strong adverse hemolytic effect. Hence, we attempted to improve the therapeutic potential of melittin-dKLA by reducing toxicity and increasing stability. Nine truncated melittin fragments were synthesized and examined. Of the nine peptides, the melittin-dKLA8-26 showed the best binding properties to M2 macrophages and discriminated M0/M1/M2. All fragments, except melittin, lost their hemolytic effects. To increase the stability of the peptide, melittin-dKLA8-26 fragment was conjugated with PEGylation at the amino terminus and was named PEG-melittin-dKLA8-26. This final drug candidate was assessed in vivo in a murine TNBC model and showed superior effects on tumor growth, survival rates, and lung metastasis compared with the previously used melittin-dKLA. Taken together, our study showed that the novel PEG-melittin-dKLA8-26 possesses potential as a new drug for treating TNBC and TNBC-mediated metastasis by targeting TAMs.
Language	English
Publishing date	2022-12-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms232415751
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Article ; Online: IL-6 produced by prostate epithelial cells stimulated with Trichomonas vaginalis promotes proliferation of prostate cancer cells by inducing M2 polarization of THP-1-derived macrophages.

Han, Ik-Hwan / Song, Hyun-Ouk / Ryu, Jae-Sook

PLoS neglected tropical diseases

2020 Volume 14, Issue 3, Page(s) e0008126

Abstract: Trichomonas vaginalis (Tv), a protozoan parasite causing sexually-transmitted disease, has been detected in tissue of prostatitis, benign prostatic hyperplasia (BPH) and prostate cancer (PCa). IL-6, a mediator of chronic inflammation, induces the ... ...

Abstract	Trichomonas vaginalis (Tv), a protozoan parasite causing sexually-transmitted disease, has been detected in tissue of prostatitis, benign prostatic hyperplasia (BPH) and prostate cancer (PCa). IL-6, a mediator of chronic inflammation, induces the progression of prostate cancer, and influences the polarization of M2 macrophages, which are the main tumor-associated macrophages. We investigated whether IL-6 produced by human prostate epithelial cells stimulated with Tv induces the M2 polarization of THP-1-derived macrophages, which in turn promotes the progression of PCa. Conditioned medium was prepared from Tv-infected (TCM) and uninfected (CM) prostate epithelial cells (RWPE-1). Thereafter conditioned medium was prepared from macrophages after incubation with CM (M-CM) or TCM (M-TCM). RWPE-1 cells infected with Tv produced IL-6 and chemokines such as CCL2 and CXCL8. When human macrophages were treated with conditioned medium of RWPE-1 cells co-cultured with Tv (TCM), they became polarized to M2-like macrophages as indicated by the production of IL-10 and TGF-β, and the expression of CD36 and arginase-1, which are M2 macrophage markers. Moreover, proliferation of the M2-like macrophages was also increased by TCM. Blockade of IL-6 signaling with IL-6 receptor antibody and JAK inhibitor (Ruxolitinib) inhibited M2 polarization of THP-1-derived macrophages and proliferation of the macrophages. To assess the effect of crosstalk between macrophages and prostate epithelial cells inflamed by Tv infection on the growth of prostate cancer (PCa) cells, PC3, DU145 and LNCaP cells were treated with conditioned medium from THP-1-derived macrophages stimulated with TCM (M-TCM). Proliferation and migration of the PCa cells were significantly increased by the M-TCM. Our findings suggest that IL-6 produced in response to Tv infection of the prostate has an important effect on the tumor microenvironment by promoting progression of PCa cells following induction of M2 macrophage polarization.
MeSH term(s)	Animals ; Cell Culture Techniques ; Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Culture Media, Conditioned ; Disease Progression ; Epithelial Cells/metabolism ; Humans ; Interleukin-6/metabolism ; Macrophages/drug effects ; Male ; Models, Theoretical ; Prostatic Neoplasms/pathology ; Prostatitis/complications ; Trichomonas Infections/complications ; Trichomonas vaginalis/immunology ; Tumor Cells, Cultured
Chemical Substances	Culture Media, Conditioned ; IL6 protein, human ; Interleukin-6
Language	English
Publishing date	2020-03-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2429704-5
ISSN	1935-2735 ; 1935-2727
ISSN (online)	1935-2735
ISSN	1935-2727
DOI	10.1371/journal.pntd.0008126
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Article ; Online: Therapeutic Effect of Melittin-dKLA Targeting Tumor-Associated Macrophages in Melanoma.

Han, Ik-Hwan / Jeong, Chanmi / Yang, Juwon / Park, Seung-Hyeok / Hwang, Deok-Sang / Bae, Hyunsu

International journal of molecular sciences

2022 Volume 23, Issue 6

Abstract: Melanoma is an immunogenic tumor and a serious type of skin cancer. Tumor-associated macrophages (TAMs) express an M2-like phenotype and are involved in all stages of melanomagenesis; it is hence a promising target for cancer immunotherapy. We herein ... ...

Abstract	Melanoma is an immunogenic tumor and a serious type of skin cancer. Tumor-associated macrophages (TAMs) express an M2-like phenotype and are involved in all stages of melanomagenesis; it is hence a promising target for cancer immunotherapy. We herein investigated whether melittin-dKLA inhibits the growth of melanoma by inducing apoptosis of M2-like macrophages. For the in vitro study, a conditioned medium of macrophages was prepared from M0, M1, or M2-differentiated THP-1 cells with and without melittin-dKLA. The affinity of melittin for M2 macrophages was studied with FITC (fluorescein isothiocyanate)-conjugated melittin. For the in vivo study, murine melanoma cells were inoculated subcutaneously in the right flank of mice, melittin-dKLA was intraperitoneally injected at 200 nmol/kg every three days, and flow cytometry analysis of TAMs was performed. Since melittin binds preferentially to M2-like macrophages, melittin-dKLA induced more caspase 3 expression and cell death in M2 macrophages compared with M0 and M1 macrophages and melanoma cells. Melittin-dKLA significantly inhibited the proliferation and migration of M2 macrophages, resulting in a decrease in melanoma tumor growth in vivo. The CD206
MeSH term(s)	Animals ; Cell Line, Tumor ; Immunotherapy/methods ; Macrophages/metabolism ; Melanoma/metabolism ; Melitten/pharmacology ; Melitten/therapeutic use ; Mice ; Tumor-Associated Macrophages
Chemical Substances	Melitten (20449-79-0)
Language	English
Publishing date	2022-03-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23063094
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Article ; Online: Melittin derived peptide-drug conjugate, M-DM1, inhibits tumor progression and induces effector cell infiltration in melanoma by targeting M2 tumor-associated macrophages.

Jeong, Chanmi / Kim, Jeongdong / Han, Ik-Hwan / Kim, Soyoung / Choi, Ilseob / Kim, Hongsung / Jeong, Jin-Hyun / Bae, Hyunsu

Frontiers in immunology

2023 Volume 14, Page(s) 1178776

Abstract: Background: Melanoma has the highest mortality rate among all the types of skin cancer. In melanoma, M2-like tumor-associated macrophages (TAMs) are associated with the invasiveness of tumor cells and a poor prognosis. Hence, the depletion or reduction ... ...

Abstract	Background: Melanoma has the highest mortality rate among all the types of skin cancer. In melanoma, M2-like tumor-associated macrophages (TAMs) are associated with the invasiveness of tumor cells and a poor prognosis. Hence, the depletion or reduction of M2-TAMs is a therapeutic strategy for the inhibition of tumor progression. The aim of this study was to evaluate the therapeutic effects of M-DM1, which is a conjugation of melittin (M), as a carrier for M2-like TAMs, and mertansine (DM1), as a payload to induce apoptosis of TAMs, in a mouse model of melanoma. Methods: Melittin and DM1 were conjugated and examined for the characterization of M-DM1 by high-performance liquid chromatography and electrospray ionization mass spectrometry. Synthesized M-DM1 were examined for Results: M-DM1 was found to specifically reduce M2-like TAMs in melanoma, which potentially leads to the suppression of tumor growth, migration, and invasion. In addition, we also found that M-DM1 improved the survival rates in a mouse model of melanoma compared to M or DM1 treatment alone. Flow cytometric analysis revealed that M-DM1 enhanced the infiltration of CD8+ cytotoxic T cells and natural killer cells (NK cells) in the tumor microenvironment. Conclusion: Taken together, our findings highlight that M-DM1 is a prospective agent with enhanced anti-tumor effects.
MeSH term(s)	Female ; Mice ; Animals ; Melitten/pharmacology ; Melitten/metabolism ; Tumor-Associated Macrophages/metabolism ; Prospective Studies ; Macrophages/metabolism ; Mice, Inbred C57BL ; Melanoma/pathology ; Tumor Microenvironment
Chemical Substances	Melitten (20449-79-0)
Language	English
Publishing date	2023-04-14
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1178776
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Article ; Online: Polarization of M2 Macrophages by Interaction between Prostate Cancer Cells Treated with Trichomonas vaginalis and Adipocytes.

Chung, Hyo-Yeoung / Kim, Jung-Hyun / Han, Ik-Hwan / Ryu, Jae-Sook

The Korean journal of parasitology

2020 Volume 58, Issue 3, Page(s) 217–227

Abstract: Trichomonas vaginalis causes inflammation of the prostate and has been detected in tissues of prostate cancers (PCa), prostatitis and benign prostatic hyperplasia. Obesity is a risk factor for PCa and causes a chronic subclinical inflammation. This ... ...

Abstract	Trichomonas vaginalis causes inflammation of the prostate and has been detected in tissues of prostate cancers (PCa), prostatitis and benign prostatic hyperplasia. Obesity is a risk factor for PCa and causes a chronic subclinical inflammation. This chronic inflammation further exacerbates adipose tissue inflammation as results of migration and activation of macrophages. Macrophages are the most abundant immune cells in the PCa microenvironment. M2 macrophages, known as Tumor-Associated Macrophages, are involved in increasing cancer malignancy. In this study, conditioned medium (TCM) of PCa cells infected with live trichomonads contained chemokines that stimulated migration of the mouse preadipocytes (3T3-L1 cells). Conditioned medium of adipocytes incubated with TCM (ATCM) contained Th2 cytokines (IL-4, IL-13). Macrophage migration was stimulated by ATCM. In macrophages treated with ATCM, expression of M2 markers increased, while M1 markers decreased. Therefore, it is suggested that ATCM induces polarization of M0 to M2 macrophages. In addition, conditioned medium from the macrophages incubated with ATCM stimulates the proliferation and invasiveness of PCa. Our findings suggest that interaction between inflamed PCa treated with T. vaginalis and adipocytes causes M2 macrophage polarization, so contributing to the progression of PCa.
MeSH term(s)	Adipocytes/immunology ; Animals ; Cell Communication/immunology ; Cell Line, Tumor ; Chemokines/immunology ; Inflammation ; Macrophages/immunology ; Male ; Mice ; Obesity ; Prostatic Neoplasms/etiology ; Prostatic Neoplasms/parasitology ; Prostatic Neoplasms/pathology ; Risk Factors ; Trichomonas vaginalis
Chemical Substances	Chemokines
Language	English
Publishing date	2020-06-26
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	286875-1
ISSN	1738-0006 ; 0023-4001
ISSN (online)	1738-0006
ISSN	0023-4001
DOI	10.3347/kjp.2020.58.3.217
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Article ; Online: TAMpepK Suppresses Metastasis through the Elimination of M2-Like Tumor-Associated Macrophages in Triple-Negative Breast Cancer.

Lee, Chanju / Kim, Soyoung / Jeong, Chanmi / Cho, Inhee / Jo, Juyeon / Han, Ik-Hwan / Bae, Hyunsu

International journal of molecular sciences

2022 Volume 23, Issue 4

Abstract: Triple-negative breast cancer (TNBC) accounts for approximately 10-15% of all breast cancer cases and is characterized by high invasiveness, high metastatic potential, relapse proneness, and poor prognosis. M2-like tumor-associated macrophages (TAMs) ... ...

Abstract	Triple-negative breast cancer (TNBC) accounts for approximately 10-15% of all breast cancer cases and is characterized by high invasiveness, high metastatic potential, relapse proneness, and poor prognosis. M2-like tumor-associated macrophages (TAMs) contribute to tumorigenesis and are promising targets for inhibiting breast cancer metastasis. Therefore, we investigated whether melittin-conjugated pro-apoptotic peptide (TAMpepK) exerts therapeutic effects on breast cancer metastasis by targeting M2-like TAMs. TAMpepK is composed of M2-like TAM binding peptide (TAMpep) and pro-apoptotic peptide d(KLAKLAK)
MeSH term(s)	Animals ; Apoptosis/drug effects ; Apoptosis/physiology ; CD8-Positive T-Lymphocytes/drug effects ; CD8-Positive T-Lymphocytes/metabolism ; Cell Line, Tumor ; Disease Models, Animal ; Female ; Lymphatic Metastasis/drug therapy ; Lymphatic Metastasis/pathology ; Melitten/pharmacology ; Mice ; Mice, Inbred BALB C ; Neoplasm Recurrence, Local/metabolism ; Neoplasm Recurrence, Local/pathology ; Peptides/pharmacokinetics ; Phagocytosis/drug effects ; Phagocytosis/physiology ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/metabolism ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/physiology ; Tumor-Associated Macrophages/drug effects ; Tumor-Associated Macrophages/metabolism ; Tumor-Associated Macrophages/pathology
Chemical Substances	Peptides ; Melitten (20449-79-0)
Language	English
Publishing date	2022-02-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23042157
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Article ; Online: Inflammatory mediators of prostate epithelial cells stimulated with Trichomonas vaginalis promote proliferative and invasive properties of prostate cancer cells.

Han, Ik-Hwan / Kim, Jung-Hyun / Jang, Ki-Seok / Ryu, Jae-Sook

The Prostate

2019 Volume 79, Issue 10, Page(s) 1133–1146

Abstract: Background: Trichomonas vaginalis (Tv) is the most common sexually transmitted parasite. It is detected in prostatic tissue of benign prostatic hyperplasia, prostatitis, and prostate cancer (PCa) and has been suggested to cause chronic prostatitis. ... ...

Abstract	Background: Trichomonas vaginalis (Tv) is the most common sexually transmitted parasite. It is detected in prostatic tissue of benign prostatic hyperplasia, prostatitis, and prostate cancer (PCa) and has been suggested to cause chronic prostatitis. Moreover, up to 20% of all cancers worldwide are associated with chronic inflammation. Here, we investigated whether inflammatory mediators produced by normal human prostate epithelial cells (RWPE-1) stimulated with Tv could promote growth and invasiveness of PCa cells. Methods: Conditioned medium of RWPE-1 cells was prepared by stimulating them with Tv (trichomonad-conditioned medium [TCM]) and without Tv (conditioned medium [CM]). Promotion of PCa cells (PC3, DU145, and LNCaP) was assessed by wound healing, proliferation, and invasion assays. Results: We observed that the production of interleukin (IL)-1β, IL-6, CCL2, CXCL8, prostaglandin-E2 (PGE Conclusions: Our results suggest that Tv infection may be one of the factors creating the supportive microenvironment to promote proliferation and invasiveness of PCa cells.
MeSH term(s)	Cell Proliferation/physiology ; Chemokine CCL2/metabolism ; Dinoprostone/metabolism ; Epithelial Cells/metabolism ; Epithelial Cells/parasitology ; Epithelial Cells/pathology ; Humans ; Inflammation/metabolism ; Inflammation/parasitology ; Inflammation/pathology ; Interleukin-1beta/metabolism ; Interleukin-6/metabolism ; Interleukin-8/metabolism ; Male ; Neoplasm Invasiveness/pathology ; Prostate/metabolism ; Prostate/parasitology ; Prostate/pathology ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/parasitology ; Prostatic Neoplasms/pathology ; Prostatitis/metabolism ; Prostatitis/parasitology ; Prostatitis/pathology ; Trichomonas Infections/metabolism ; Trichomonas Infections/pathology ; Trichomonas vaginalis
Chemical Substances	CXCL8 protein, human ; Chemokine CCL2 ; IL1B protein, human ; Interleukin-1beta ; Interleukin-6 ; Interleukin-8 ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2019-05-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604707-5
ISSN	1097-0045 ; 0270-4137
ISSN (online)	1097-0045
ISSN	0270-4137
DOI	10.1002/pros.23826
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Article ; Online: Magnoliae Cortex Alleviates Muscle Wasting by Modulating M2 Macrophages in a Cisplatin-Induced Sarcopenia Mouse Model.

Hong, Minwoo / Han, Ik-Hwan / Choi, Ilseob / Cha, Nari / Kim, Woojin / Kim, Sun Kwang / Bae, Hyunsu

International journal of molecular sciences

2021 Volume 22, Issue 6

Abstract: Cachexia causes high mortality, low quality of life, and rapid weight loss in cancer patients. Sarcopenia, a condition characterized by the loss of muscle, is generally present in cachexia and is associated with inflammation. M2 macrophages, also known ... ...

Abstract	Cachexia causes high mortality, low quality of life, and rapid weight loss in cancer patients. Sarcopenia, a condition characterized by the loss of muscle, is generally present in cachexia and is associated with inflammation. M2 macrophages, also known as an anti-inflammatory or alternatively activated macrophages, have been shown to play a role in muscle repair. Magnoliae Cortex (M.C) is a widely used medicinal herb in East Asia reported to have a broad range of anti-inflammatory activities; however, the effects of M.C on sarcopenia and on M2 macrophage polarization have to date not been studied. This study was designed to investigate whether the oral administration of M.C could decrease cisplatin-induced sarcopenia by modulating M2 macrophage polarization in mice. C57BL/6 mice were injected intraperitoneally with cisplatin (2.5 mg/kg) to mimic chemotherapy-induced sarcopenia. M.C extract (50, 100, and 200 mg/kg) was administered orally every 3 days (for a total of 12 times). M.C (100 and 200 mg/kg) significantly alleviated the cisplatin-induced loss of body mass, skeletal muscle weight, and grip strength. In addition, M.C increased the expression of M2 macrophage markers, such as MRC1, CD163, TGF-β, and Arg-1, and decreased the expression of M1-specific markers, including NOS2 and TNF-α, in skeletal muscle. Furthermore, the levels of like growth factor-1(IGF-1), as well as the number of M2a and M2c macrophages, significantly increased in skeletal muscle after M.C administration. M.C did not interfere with the anticancer effect of cisplatin in colon cancer. Our results demonstrated that M.C can alleviate cisplatin-induced sarcopenia by increasing the number of M2 macrophages. Therefore, our findings suggest that M.C could be used as an effective therapeutic agent to reverse or prevent cisplatin-induced sarcopenia.
MeSH term(s)	Animals ; Biomarkers ; Cisplatin/adverse effects ; Disease Models, Animal ; Insulin-Like Growth Factor I/genetics ; Insulin-Like Growth Factor I/metabolism ; Macrophage Activation/drug effects ; Macrophages/drug effects ; Macrophages/metabolism ; Magnolia/chemistry ; Mice ; Molecular Structure ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscular Atrophy/drug therapy ; Muscular Atrophy/metabolism ; Muscular Atrophy/pathology ; Plant Extracts/chemistry ; Plant Extracts/pharmacology ; Sarcopenia/drug therapy ; Sarcopenia/etiology ; Sarcopenia/metabolism ; Sarcopenia/pathology
Chemical Substances	Biomarkers ; Plant Extracts ; Insulin-Like Growth Factor I (67763-96-6) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2021-03-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22063188
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