Introduction: Bekam, an Islamic variant of cupping, is an ancient form of traditional medicine still practised today in Malaysia. There are published findings indicating that cupping benefits patients with low back pain, other musculoskeletal pain and even pain from cancer, herpes zoster and trigeminal neuralgia when pain is measured on an analogue scale. We proposed to investigate whether in addition to pain improvement on an analogue scale we could show if pain relief might be demonstrated in terms of reduction of analgesic use. Methods: We carried out a retrospective cross sectional study on subjects who had been for outpatient clinic treatment with chronic pain of at least one month and who completed at least two bekam therapy sessions. In addition to documenting a pain score before and after therapy we documented their analgesic consumption. Results: A total of 77 respondents, with overlapping symptoms of headache, backache and joint pains were included. The mean pain score before bekam therapy was 6.74±1.78, and was 2.66±1.64 after two sessions of therapy. Twenty eight respondents completed six sessions of bekam therapy and had a mean pain score of 2.25±1.32 after. Thirty-four patients consumed analgesic medication before starting bekam therapy and only twelve did so after. The consumption of analgesics was significantly lower after bekam therapy. Conclusions: Bekam therapy appears to help patients experience less pain and reduce the amount of analgesic medication they consume. Nevertheless only a randomised prospective study will eliminate the biases a retrospective study is encumbered with and we believe would be worth doing.
Medicine, Traditional ; Chronic Pain

Hepatic stellate cells(HSCs)are essential drivers of fibrogenesis.Inducing activated-HSC apoptosis is a promising strategy for treating hepatic fibrosis.18beta-glycyrrhetinic acid(18β-GA)is a natural com-pound that exists widely in herbal medicines,such as Glycyrrhiza uralensis Fisch,which is used for treating multiple liver diseases,especially in Asia.In the present study,we demonstrated that 18β-GA decreased hepatic fibrosis by inducing the apoptosis in activated HSCs.18β-GA inhibited the expression of α-smooth muscle actin and collagen type Ⅰ alpha-1.Using a chemoproteomic approach derived from activity-based protein profiling,together with cellular thermal shift assay and surface plasmon reso-nance,we found that 18β-GA covalently targeted peroxiredoxin 1(PRDX1)and peroxiredoxin 2(PRDX2)proteins via binding to active cysteine residues and thereby inhibited their enzymatic activities.18β-GA induced the elevation of reactive oxygen species(ROS),resulting in the apoptosis of activated HSCs.PRDX1 knockdown also led to ROS-mediated apoptosis in activated HSCs.Collectively,our findings revealed the target proteins and molecular mechanisms of 18β-GA in ameliorating hepatic fibrosis,highlighting the future development of 18β-GA as a novel therapeutic drug for hepatic fibrosis.

In an effort to understand the molecular events contributing to the cytotoxicity activity of resveratrol (RSV), we investigated its effects on human lung adenocarcinoma epithelial cell line A549 at different concentrations. Cellular nucleoside metabolic profiling was determined by an established liquid chromatography-mass spectrometry method in A549 cells. RSV resulted in significant decreases and imbalances of deoxyribonucleoside triphosphates (dNTPs) pools suppressing subsequent DNA synthesis. Meanwhile, RSV at high concentration caused significant cell cycle arrest at S phase, in which cells required the highest dNTPs supply than other phases for DNA replication. The inhibition of DNA synthesis thus blocked subsequent progression through S phase in A549 cells, which may partly contribute to the cytotoxicity effect of RSV. However, hydroxyurea (HU), an inhibitor of RNR activity, caused similar dNTPs perturbation but no S phase arrest, finally no cytotoxicity effect. Therefore, we believed that the dual effect of high concentration RSV, including S phase arrest and DNA synthesis inhibition, was required for its cytotoxicity effect on A549 cells. In summary, our results provided important clues to the molecular basis for the anticancer effect of RSV on epithelial cells.