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Transient receptor potential (TRP) vanilloid 4 (TRPV4) is a member of the Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -permeable TRP superfamily. Resveratrol (RESV) has been extensively utilized in TRP channel regulation due to its pharmacological properties, which include antioxidant and TRP inhibitory effects. The protective function of RESV and the contribution of TRPV4 to streptozotocin (STZ)-induced neuropathic pain in mice are still unclear. Here, we evaluated the effects of RESV through the modulation of TRPV4 on Ca\n                    <jats:sup>2+<\/jats:sup>\n                    influx, ROS-mediated pain, apoptosis, and oxidative damage in the mouse dorsal root ganglion (DRGs). From the 32 mice, four groups were induced: control, RESV, STZ, and STZ\u2009+\u2009RESV. We found that the injection of RESV reduced the changes caused by the STZ-induced stimulation of TRPV4, which in turn increased mechanical\/thermal neuropathic pain, cytosolic Ca\n                    <jats:sup>2+<\/jats:sup>\n                    influx, TRPV4 current density, oxidants (lipid peroxidation, mitochondrial ROS, and cytosolic ROS), and apoptotic markers (caspase-3, -8, and -9). The RESV injection also increased the STZ-mediated reduction of viability of DRG and the amounts of glutathione, glutathione peroxidase, vitamin A, \u03b2-carotene, and vitamin E in the brain, erythrocytes, plasma, liver, and kidney. All of these findings suggest that TRPV4 stimulation generates oxidative neurotoxicity, neuropathic pain, and apoptosis in the STZ-induced diabetic mice. On the other hand, neurotoxicity and apoptosis were reduced due to the downregulation of TRPV4 carried out through the RESV injection.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Graphical Abstract<\/jats:bold>\n                  <\/jats:p>\n                  <jats:p>\n                    An overview of how resveratrol (RESV) inhibits TRPV4 in mice to modulate the effects of diabetes mellitus-induced diabetic peripheral neuropathy (DPN). Ruthenium red (RuR) inhibits TRPV4, while GSK1016790A (GSK) and reactive free oxygen radicals (ROS) activate it. In the mitochondria of DRGs, the glucose oxidation brought on by diabetes mellitus (STZ) causes an intracellular free Ca\n                    <jats:sup>2+<\/jats:sup>\n                    and Zn\n                    <jats:sup>2+<\/jats:sup>\n                    influx excess that is dependent on TRPV4. The administration of STZ leads to the DRG becoming more depolarized (\u0394\u03a8m), which in turn causes an increase in mitochondrial ROS, apoptosis, and caspases (caspase-3, caspase-8, and caspase-9) by downregulating enzymatic (glutathione peroxidase, GSH-Px) and non-enzymatic (glutathione (GSH), vitamin A, and vitamin E) antioxidants. The mice\u2019s molecular pathways were diminished by the RESV injections. (Increase (\u2191); diminish (\u2193))\n                  <\/jats:p>","DOI":"10.1007\/s12035-024-04311-4","type":"journal-article","created":{"date-parts":[[2024,7,8]],"date-time":"2024-07-08T03:02:10Z","timestamp":1720407730000},"page":"7269-7286","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["Resveratrol Modulates Diabetes-Induced Neuropathic Pain, Apoptosis, and Oxidative Neurotoxicity in Mice Through TRPV4 Channel Inhibition"],"prefix":"10.1007","volume":"61","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8622-6072","authenticated-orcid":false,"given":"Haci \u00d6mer","family":"Osmanl\u0131o\u011flu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0887-6974","authenticated-orcid":false,"given":"Mustafa","family":"Naz\u0131ro\u011flu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,7,8]]},"reference":[{"key":"4311_CR1","doi-asserted-by":"publisher","first-page":"3425617","DOI":"10.1155\/2016\/3425617","volume":"2016","author":"LM Rom\u00e1n-Pintos","year":"2016","unstructured":"Rom\u00e1n-Pintos LM, Villegas-Rivera G, Rodr\u00edguez-Carrizalez AD, Miranda-D\u00edaz AG, Cardona-Mu\u00f1oz EG (2016) Diabetic polyneuropathy in type 2 diabetes mellitus: inflammation, oxidative stress, and mitochondrial function. 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According to the guidelines established by MAKU, each experiment was assessed and approved by the Local Animal Care Committee of MAKU (date, 17.11.2022; meeting number, 108; decision number, 993; owner, Dr. Haci \u00d6mer Osmanl\u0131o\u011flu).","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics Approval"}},{"value":"Mustafa Naz\u0131ro\u011flu looked over the most recent research. The project was designed by Mustafa Naz\u0131ro\u011flu and Haci \u00d6mer Osmanl\u0131o\u011flu. Haci \u00d6mer Osmanl\u0131o\u011flu conducted plate reader tests and animal care. Mustafa Naz\u0131ro\u011flu investigated and edited the article after generating this perspective article. The submitted final manuscript was approved by all authors.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent to Participate"}},{"value":"The presented final manuscript was approved by all authors<b>.<\/b>","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent for Publication"}},{"value":"The authors declare no competing interests.","order":5,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing Interests"}},{"value":"The treatments and animal tissue samples in the current study were started using MAKU. Dr. M. Naz\u0131ro\u011flu can provide the results of the analyses upon request. BSN Health, Analyses, Innovation, Consultancy, Organization, Agriculture, and Industry Ltd. (G\u00f6ller B\u00f6lgesi Teknokenti, Isparta, T\u00fcrkiye) was the location of the analyses. All the visuals in the manuscript, including the graphical abstract, were prepeared by the communication author (MN).","order":6,"name":"Ethics","group":{"name":"EthicsHeading","label":"Accessibility of Information and Resources"}}]}}