Retinal inflammation is a devastating pathological process in ocular diseases. Functional impairment of retinal pigment epithelium (RPE) is associated with inflammatory retinal diseases. Enhancing the protective axis namely ACE2/Ang-(1-7)/Mas by activation of ACE2 presents anti-inflammatory properties. We investigated whether diminazene aceturate (DIZE), an angiotensin-converting enzyme 2 (ACE2) activator, prevented lipopolysaccharide (LPS)-induced inflammatory response by activating the protective axis and whether the effect was mediated by inhibiting the mitogen-activated protein kinase (MAPK) and the nuclear factor-κB (NF-κB) pathways. Cell counting kit-8 (CCK-8) assay and real-time PCR were used to determine the optimum concentration and incubation time of DIZE. ARPE-19 cells and primary cultured human retinal pigment epithelia (hRPE) were incubated with or without 10 μg/mL DIZE for 6 h before stimulated with 5 μg/mL LPS for 24 h. The mRNA expression of inflammatory cytokines, AT1R, and AT2R was analyzed. The protein level of inflammatory cytokines, Ang II, and Ang-(1-7) was detected. Phosphorylation of p38 MAPK, extracellular signal-regulated kinase (ERK)1/2, c-Jun N-terminal kinase (JNK) and phosphorylated transcription inhibition factor-κB-α (p-IκB-α) were measured. Inhibitors of MAPKs and NF-κB were added to verify the involvement of these pathways. A small interfering RNA (siRNA) targeted to ACE2 and a selective Ang-(1-7) antagonist A779 was used to confirm the role of ACE2 and the involvement of ACE2/Ang-(1-7)/Mas axis. DIZE remarkably increased the expression of ACE2 and inhibited the expression of IL-6, IL-8, and MCP-1 at both mRNA and protein levels in both RPE cell lines stimulated with LPS. Inhibitors of p38, ERK1/2, JNK, and NF-κB significantly decreased LPS-induced overproduction of IL-6, IL-8, and MCP-1. DIZE reduced the expression of Ang II and AT1R, whereas increased Ang-(1-7). Furthermore, DIZE downregulated the phosphorylation of p38MAPK, ERK1/2, JNK, and the activation of NF-κB upon stimulation with LPS. Downregulating ACE2 and pre-treatment with A779 abrogated the effects of DIZE on production of cytokines, the expression of Ang II, Ang-(1-7), AT1R, phosphorylation of MAPKs and activation of NF-κB. DIZE inhibits LPS-induced inflammatory response by activating ACE2/Ang-(1-7)/Mas axis in human RPE cells. The protective effect is mediated by inhibiting the p38MAPK, ERK1/2, JNK, and NF-κB pathways.

To report a case of macular injury caused by short-term exposure to a handheld high-intensity light emitting diode (LED) light. Interventional case report. A patient with macular injury caused by short-term exposure to the light of a handheld high-intensity LED device. The patient was examined and followed for 3 months after exposure with ophthalmologic examinations (including funduscopy, optical coherence tomography [OCT], fluorescein angiography [FA], and multifocal electroretinography [mfERG]). The injured eye was treated with one retrobulbar injection of 20 mg triamcinolone acetonide at 5 days after exposure. Visual acuity, ophthalmoscopic, and OCT findings. 3 days after exposure, the best corrected visual acuity (BCVA) of the right eye was 6/20. OCT revealed the acute stage of the injury with eminence of the retinal pigment epithelium (RPE). BCVA was improved to 16/20 and 20/20 at 19 and 33 days after exposure, respectively. OCT results of follow-ups at five days, 19 days, 33 days and 3 months after exposure have demonstrated the restoration process of the injury. Short-term exposure to high-intensity LED light may cause damage to the retina. As the expansion of LED use in modern life, education and supervision are of urgent need for public health.

The Nd:YAG laser is widely used in various aspects of work and life. Currently, it has become a popular cosmetic technique in beauty salons. The laser can be dangerous when it flashes into people's eyes. A 34-year-old female sustained a 1064-nm Q-switched Nd:YAG laser injury to her left eye. One month after the injury, she presented to our clinic with best-corrected visual acuity (BCVA) of 20/250 and a full-thickness macular hole on the optical coherence tomography (OCT). The patient received pars plana vitrectomy, internal limiting membrane peeling and sterile air injection 3 months after the injury. OCT showed closure of the hole 9 days postoperatively. After a 3-month follow-up, her BCVA improved to 20/100. This case report comprehensively introduces the whole progression of a cosmetic laser-induced macular hole from formation to recovery. Due to the potential threats of the laser and its irreversible damage to the retina and choroid, sufficient education should be given before performing any laser devices, especially those without professional knowledge.