Photodynamic　therapy　(PDT)　is　a　new　therapy　for　treating　cancer　with　less　toxicity,　high　selectivity,　good　cooperativity,　and　repetitive　usability.　However,　keloid　treatment　by　PDT　is　mainly　focused　on　clinical　appearance,　and　few　studies　have　been　conducted　on　the　mechanisms　of　PDT.　In　this　study,　key　factors　of　the　classical　mitochondrial　apoptosis　signaling　pathway　were　measured　to　assess　the　effect　of　a　new　PDT　photosensitizer　(p1).　A　specific　inhibitor　of　caspase-8　(Z-IETD-FMK)　was　also　used　to　verify　the　possible　mechanisms.　Twelve　samples　were　obtained　from　12　patients　(six　with　keloids　and　six　without)　selected　randomly　from　the　Department　of　Plastic　Surgery　at　Peking　Union　Medical　College　Hospital　from　January　to　December　2020.　After　cell　culture,　fibroblasts　were　divided　into　13　groups.　The　morphology　of　fibroblasts　in　each　group　was　observed　by　microscopy.　Cell　activity　was　measured　by　cell　counting　kit-8,　and　cell　apoptotic　morphology　was　observed　by　TUNEL　staining.　The　reactive　oxygen　species　(ROS)　relative　value　was　measured　by　a　ROS　test　kit.　The　expression　levels　of　key　mitochondrial　factors　(caspase-3,　caspase-8,　cytochrome-c,　Bax,　and　Bcl-2)　were　assessed　by　western　blot,　and　mRNA　expression　of　caspase-3　and　caspase-8　was　measured　by　RT-qPCR.　We　showed　that　p1　had　a　satisfactory　proapoptotic　effect　on　keloid　fibroblasts　by　increasing　the　expression　of　ROS,　caspase-3,　caspase-8,　and　cytochrome-c,　and　decreasing　the　Bcl-2/Bax　ratio;　however,　this　effect　was　partially　inhibited　by　Z-IETD-FMK,　indicating　that　caspase-8　may　be　one　of　the　p1＇s　targets　to　achieve　the　proapoptotic　effect.