Effectiveness of Xielikang capsules in treating HIV-related diarrhea by increasing the plasma concentration of interleukin-17.

OBJECTIVE: To evaluate the efficacy of Xielikang capsules (XLKC) in the treatment of HIV-related diarrhea (HRD) and its effect on the plasma concentration of interleukin-17 (IL-17). METHODS: This was a randomized, open-label, positively-controlled clinical trial. Sixty-seven HRD patients were randomly assigned to two groups: one group was treated with XLKC (n = 35), the other with diosmectite (Smecta®, n = 32). All patients were treated for 4 weeks. The HRD symptom scores were evaluated in each patient based on the frequency of diarrhea, and the quality and shape of the stool according to the Chinese Medicine Clinical Treatment of AIDS Program. The plasma concentration of IL-17 before and after treatment was measured with ELISA. RESULTS: Compared with the Smecta® group, the XLKC group had a significantly reduced frequency of diarrhea and HRD symptom score regarding the quality and shape of stools (P < 0.05). The IL-17 concentration in the peripheral blood of the XLKC group was significantly increased after treatment, while the IL-17 concentration in the Smecta® group significantly decreased after treatment. CONCLUSION: XLKC improves the symptoms of patients with HRD, and increases the plasma concentration of IL-17.

miR-135a acts as a tumor suppressor in gastric cancer in part by targeting KIFC1.

miR-135a was downregulated in the majority of human primary gastric cancer (GC) tissues and GC cell lines. Kinesin family member C1 (KIFC1) was significantly upregulated in GC tissues and cell lines and promoted GC development and progression. We searched for miR-135a targets by using MiRanda, TargetScan, and PicTar tools, and found that KIFC1 was a potential target of miR-135a. Based on these findings, we speculated that miR-135a might target KIFC1 to inhibit GC growth. We determined the expression of miR-135a and KIFC1 by quantitative real-time polymerase chain reaction and Western blot assays, respectively, and found downregulation of miR-135a and upregulation of KIFC1 in GC tissues and cell lines. Cell proliferation and apoptosis assays showed that knockdown of KIFC1 inhibited proliferation and promoted apoptosis of GC cells, and miR-135a mimics had similar effects on GC cell proliferation and apoptosis. Furthermore, we verified that KIFC1 was a direct target of miR-135a, which confirmed our speculation that the functional effect of miR-135a on GC cells, at least, in part, depends on KIFC1. These findings suggest that miR-135a has an important role in the suppression of GC and presents a novel mechanism of miRNA-mediated KIFC1 expression in cancer cells.