Retinitis pigmentosa (RP) represents a clinically and genetically heterogeneous disease characterized by progressive photoreceptor loss. In recent years, research has been rarely made in blood flow affected in RP. The specific mechanism of blood flow affected in RP is not completely clear. A number of studies indicated that the decreased blood flow was related to RP. According to clinical observation and treatment experience, Chinese medicine considered that blood stasis runs throughout the RP disease progression, and the blood stasis corresponding to Chinese herbal medicine has a positive effect on the clinical treatment of RP. Therefore, we proposed that the decreased blood flow may participate in the lesion. In this article, we will review the findings on the decreased blood flow affected in RP from the perspective of modern medicine and Chinese medicine.

Background. Administration of nonsteroidal anti‐inflammatory drugs (NSAIDs) often causes small intestinal ulcers in patients, but few effective drugs are currently available to manage such serious adverse events of NSAIDs. Li‐Zhong decoction (LZD), a well‐known traditional Chinese medicine (TCM) formula, is commonly prescribed for treatment of gastrointestinal diseases. The present study aimed to investigate the anti‐ulcerogenic activity of LZD on indomethacin‐ (IND‐) induced duodenal ulcer in rats. Mechanistic studies of action of LZD were focused on involvement of TLR‐2/MyD88 signaling pathway. Methods. Fifty male Sprague‐Dawley (SD) rats were randomly and evenly divided into five groups: normal control, ulcer control (IND, 25 mg/kg), IND + esomeprazole (ESO, 4.17 mg/kg), and IND + low and high doses of LZD (3.75 and 7.50 g/kg). Macroscopic and histopathological examinations were performed for evaluation of ulcer index (UI), curative index (CI), and microscopic score (MS). Levels of duodenal inflammatory biomarkers and cytoprotective mediators including interleukin‐4 (IL‐4), IL‐10, tumor necrosis factor‐α (TNF‐α), and prostaglandin E₂ (PGE₂) were measured by ELISA. Expression levels of TLR‐2 and MyD88 mRNA were assessed by qRT‐PCR. The expression and distribution of TLR‐2 and MyD88 proteins were analyzed by western blot and immunohistochemistry, respectively. Results. Gross and microscopic examinations of the IND‐treated rats revealed severe duodenal hemorrhagic necrosis, inflammatory infiltration, villus destruction, and crypt abscess, while LZD‐treated rats manifested these pathological events to a markedly lesser degree. LZD significantly decreased UI and MS, increased CI, preserved the integrity of the villus and crypt, and normalized the tissue architecture of the duodenum of rats. The elevated TNF‐α levels in the IND‐treated rats were markedly diminished in the LZD‐treated rats, while lower levels of IL‐4, IL‐10, and PGE₂ observed in IND‐treated rats were significantly increased in LZD‐treated rats. Interestingly, improvement of immune function in duodenal mucosa by reduction of mRNA and protein expression levels of TLR‐2 and MyD88 was also observed in rats treated with LZD. Consistently, immunohistochemical analyses revealed a lower co‐localization of TLR‐2 and MyD88 proteins in the duodenal mucosa of LZD‐treated rats as compared to the IND‐induced rats. Conclusions. Our data demonstrate that LZD protects the duodenal mucosa from IND‐caused lesions, which is at least partially attributable to the interaction of its potential cytoprotective and anti‐inflammatory mechanisms together with enhancement of the mucosal immunity through TLR‐2/MyD88 signaling pathway.

Background: Linarine is a natural chemical component widely found in Buddleja officinalis Maxim., Chrysanthemum indicum L., Mentha canadensis L., and other medicinal plants. Modern pharmacological studies have shown that linarine with good anti-inflammatory and antioxidant activities can inhibit the proliferation and induce apoptosis of many kinds of tumor cells. Moreover, linarine showed protective effect on the liver, kidneys, and other organs.Methods: Inflammation model of human corneal epithelial cell (HCEC) was constructed using NaCl induction, and cytotoxicity was detected by the CCK8 assay. The levels of inflammatory factors tumor necrosis factor-α (TNF-α) and interleukin 1β (IL-1β) were measured using Enzyme-linked immunoassay (ELISA). Chronic painful stimulation (tail clamping) in combination with Benzalkonium Chloride Solution drops in a desiccator established a mouse model of dry eye disease (DED). The following parameters were recorded: body mass, anal temperature, tear secretion, tear film rupture time, and corneal fluorescein staining. The levels of inflammatory factors mitogen activated protein kinase (MAPK), nuclear factor kappa-B (NF-kB), c-Jun N-terminal kinase (JNK), IL-1β, Interleukin 18(IL-18), A2A, A3, P2X4, P2X7, P2Y1 were measured by using immunofluorescence (IF) staining.Results: Linarine can inhibit the secreation of TNF-α, and IL-1β in HCECs. Linarine prolonged tear film rupture time, promoted tear secretion, repaired corneal damage, and reduced the levels of inflammatory factors of MAPK, NF-kB, JNK, IL-1β, IL-18, and modulated the levels of the purinergic receptor.Conclusions: Linarine is effective in treating dry eye in mice by inhibiting purinergic receptors-mediated inflammatory response.