ABSTRACTThis study investigated the effect of 8 weeks of high‐intensity interval training (HIIT) on oxidative stress, inflammation, and apoptosis in rats with type 2 diabetes (T2D), focusing on the role of the Humanin (HN). In this study, 28 male Wistar rats were assigned to one of four groups: healthy control (CO), diabetes control (T2D), exercise (EX), and diabetes + exercise (T2D + EX). After diabetes induction (2‐month high‐fat diet and injection of 35 mg/kg streptozotocin), the animals in the EX and T2D + EX groups underwent an 8‐week HIIT protocol (4–10, interval of 80%–100% of maximum speed). HOMA‐IR, fasting blood glucose, and HN levels were measured in the serum. The expression of HN, Bax, Bcl‐2, CAT, GPx, MDA, TNFα, and IL‐10 was measured in the soleus muscle. Our results showed that the serum level of HN and the muscle levels of IL‐10, SOD, CAT, and Bax were higher in the T2D + EX group than in the T2D group. However, the HOMA‐IR index and the muscle levels of MDA, TNFα, and Bcl‐2 were lower in the T2D + EX group than in the T2D group. Muscle levels of HN and GPx showed no significant difference between the T2D + EX and T2D groups. The result of Pearson analysis showed a significant correlation between HN and MDA, SOD, Bax and Bcl‐2. This study provides evidence that there is a correlation between serum Humanin levels and HIIT. HIIT benefits T2D rats by reducing inflammation and oxidative stress. Given Humanin's established involvement in inflammation and oxidative stress, it is possible that the benefits of HIIT on T2D rats are mediated by humanin.

01 Feb 2025·Neuropharmacology

Humanin attenuates metabolic, toxic, and traumatic neuropathic pain in mice by protecting against oxidative stress and increasing inflammatory cytokine

Article

Author: Bilgin, Batuhan ; Bulut, Ferah ; Adam, Muhammed ; Kelestemur, Muhammed Mirac ; Ayar, Ahmet ; Canpolat, Sinan ; Ozcan, Mete ; Hekim, Munevver Gizem ; Ozcan, Sibel

Neuropathic pain is associated with diverse etiologies, including sciatica, diabetes, and the use of chemotherapeutic agents. Despite the varied origins, mitochondrial dysfunction, oxidative stress, and inflammatory cytokines are recognized as key contributing factors in both the initiation and maintenance of neuropathic pain. The effects of the mitochondrial-derived peptide humanin on neuropathic pain, however, remain unclear, despite its demonstrated influence on these mechanisms in numerous disease models. This study aimed to evaluate the effects of humanin on pain behavior in murine models of metabolic (streptozotocin/STZ), toxic (oxaliplatin/OXA), traumatic (sciatic nerve cuffing/cuff), and neuropathic pain. A secondary objective was to assess whether humanin modulates oxidative damage and inflammatory cytokine levels in these neuropathic pain models. Humanin (4 mg/kg) was administered intraperitoneally (i.p.) to BALB/c male mice with induced neuropathic pain over a period of 15 days, with pain thresholds assessed using hot plate, cold plate, and Von Frey tests. Serum levels of antioxidant enzymes, oxidative stress markers, and inflammatory/anti-inflammatory cytokines were measured via enzyme-linked immunosorbent assay (ELISA). In neuropathic pain-induced mice, humanin administration resulted in a statistically significant increase in pain threshold values in the STZ + Humanin, OXA + Humanin, and cuff + Humanin groups compared to their respective control groups (P < 0.05) over 15 days. Furthermore, humanin treatment significantly elevated antioxidant enzyme levels and anti-inflammatory cytokine concentrations, while reducing oxidative stress markers and pro-inflammatory cytokine levels compared to control groups (P < 0.01). These findings suggest that humanin exhibits therapeutic potential in the treatment of neuropathic pain induced by STZ, OXA, and cuff models. The ability of humanin to mitigate neuropathic pain through the suppression of oxidative stress and inflammatory cytokines indicates its promise as a novel therapeutic strategy.

03 Mar 2024·Free Radical Research

Humanin inhibits lymphatic endothelial cells dysfunction to alleviate myocardial infarction-reperfusion injury via BNIP3-mediated mitophagy

Article

Author: Yang, Xiaohua ; Wang, Kai ; Zou, Cao ; Guo, Lina ; Chen, Lu

OBJECTIVEAcute myocardial infarction (AMI) ranks among the top contributors to sudden death and disability worldwide. It should be noted that current therapies always cause increased reperfusion damage. Evidence suggests that humanin (HN) reduces mitochondrial dysfunction to have cardio-protective effects against MI-reperfusion injury. In this context, we hypothesized that HN may attenuate MI-reperfusion injury by alleviating lymphatic endothelial cells dysfunction through the regulation of mitophagy.MATERIALS AND METHODSIn this study, primary lymphatic endothelial cells were selected as the experimental model. Cells were maintained under 1% O₂ to induce a hypoxic phenotype. For in vivo experiments, the left coronary arteries of C57/BL6 mice were clamped for 45 min followed by 24 h reperfusion to develop MI-reperfusion injury. The volume of infarcted myocardium in MI-reperfusion injury mouse models were TTC staining. PCR and western blot were used to quantify the expression of autophagy-, mitophagy- and mitochondria-related markers. The fibrosis and apoptosis in the ischemic area were evaluated for Masson staining and TUNEL respectively. We also used western blot to analyze the expression of VE-Cadherin in lymphatic endothelial cells.RESULTSWe firstly exhibited a specific mechanism by which HN mitigates MI-reperfusion injury. We demonstrated that HN effectively reduces such injury in vivo and also inhibits dysfunction in lymphatic endothelial cells in vitro. Importantly, this inhibitory effect is mediated through BNIP3-associated mitophagy.CONCLUSIONSIn conclusion, HN alleviates myocardial infarction-reperfusion injury by inhibiting lymphatic endothelial cells dysfunction, primarily through BNIP3-mediated mitophagy.

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Indication	Highest Phase	Country/Location	Organization	Date
Myocardial Reperfusion Injury	Preclinical	China	The First Affiliated Hospital of Soochow University	27 Mar 2024
Alzheimer Disease	Preclinical	United States	CohBar, Inc.	-
Atherosclerosis	Preclinical	United States	CohBar, Inc.	-
Diabetes Mellitus, Type 2	Preclinical	United States	CohBar, Inc.	-
Toxicity	Preclinical	United States	CohBar, Inc.	-

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